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Potassium channel
In the field of cell biology, potassium channels are the most widely distributed type of ion channel and are found in virtually all living organisms.[1] They form potassium-selective pores that span cell membranes. Furthermore potassium channels are found in most cell types and control a wide variety of cell functions.[2][3]
Potassium channels function to conduct potassium ions down their electrochemical gradient, doing so both rapidly (up to the diffusion rate of K+ ions in bulk water) and selectively (excluding, most notably, sodium despite the sub-angstrom difference in ionic radius). Biologically, these channels act to set or reset the resting potential in many cells. In excitable cells, such as neurons, the delayed counterflow of potassium ions shapes the action potential.
By contributing to the regulation of the action potential duration in cardiac muscle, malfunction of potassium channels may cause life-threatening arrhythmias. Potassium channels may also be involved in maintaining vascular tone.
They also regulate cellular processes such as the secretion of hormones (e.g., insulin release from beta-cells in the pancreas) so their malfunction can lead to diseases (such as diabetes).
There are four major classes of potassium channels:
- Calcium-activated potassium channel - open in response to the presence of calcium ions or other signalling molecules.
- Inwardly rectifying potassium channel - passes current (positive charge) more easily in the outward direction (outside of the cell).
- Tandem pore domain potassium channel - are constitutively open or possess high basal activation, such as the "resting potassium channels" or "leak channels" that set the negative membrane potential of neurons.
- Voltage-gated potassium channel - are voltage-gated ion channels that open or close in response to changes in the transmembrane voltage.
The following table contains a comparison of the major classes of potassium channels with representative examples (for a complete list of channels within each class, see the respective class pages).
|Inwardly rectifying
|Tandem pore domain
Potassium channels have a tetrameric structure in which four identical protein subunits associate to form a fourfold symmetric (C4) complex arranged around a central ion conducting pore (i.e., a homotetramer). Alternatively four related but not identical protein subunits may associate to form heterotetrameric complexes with pseudo C4 symmetry. All potassium channel subunits have a distinctive pore-loop structure that lines the top of the pore and is responsible for potassium selective permeability.
There are over 80 mammalian genes that encode potassium channel subunits. However potassium channels found in bacteria are amongst the most studied of ion channels, in terms of their molecular structure. Using X-ray crystallography,[23][24] profound insights have been gained into how potassium ions pass through these channels and why (smaller) sodium ions do not.[25] The 2003 Nobel Prize for Chemistry was awarded to Rod MacKinnon for his pioneering work in this area.[26]
Selectivity filter[edit]
Potassium ion channels remove the hydration shell from the ion when it enters the selectivity filter. The selectivity filter is formed by a highly conserved five residue sequence (TVGYG, termed the signature sequence) in the P loop of each subunit, which have their electro-negative carbonyl oxygen atoms aligned toward the centre of the filter pore and form a square anti-prism similar to a water-solvating shell around each potassium binding site. The distance between the carbonyl oxygens and potassium ions in the binding sites of the selectivity filter is the same as between water oxygens in the first hydration shell and a potassium ion in water solution, providing an energetically favorable route for de-solvation of the ions. The selectivity filter opens towards the extracellular solution, exposing four carbonyl oxygens in a glycine residue (Gly79 in KcsA). The next residue toward the extracellular side of the protein is the negatively charged Asp80 (KcsA). This residue together with the five filter residues form the pore that connects the water-filled cavity in the centre of the protein with the extracellular solution.[28]
Selectivity mechanism[edit]
The mechanism of potassium channel selectivity remains under continued debate. The carbonyl oxygens are strongly electro-negative and cation-attractive. The filter can accommodate potassium ions at 4 sites usually labelled S1 to S4 starting at the extracellular side. In addition, one ion can bind in the cavity at a site called SC or one or more ions at the extracellular side at more or less well-defined sites called S0 or Sext. Several different occupancies of these sites are possible. Since the X-ray structures are averages over many molecules, it is, however, not possible to deduce the actual occupancies directly from such a structure. In general, there is some disadvantage due to electrostatic repulsion to have two neighboring sites occupied by ions. Proposals for the mechanism of selectivity have been made based on molecular dynamics simulations, toy models of ion binding, thermodynamic calculations, and structural differences between selective and non-selective channels.
The mechanism for ion translocation in KcsA has been studied extensively by simulation techniques. A complete map of the free energies of the 24=16 states (characterized by the occupancy of the S1, S2, S3, and S4 sites) has been calculated with molecular dynamics simulations, resulting in the prediction of an ion conduction mechanism in which the two doubly occupied states (S1, S3) and (S2, S4) play an essential role. The two extracellular states, Sext and S0, were found in a better resolved structure of KcsA at high potassium concentration. In free energy calculations, the entire ionic pathway from the cavity through the four filter sites out to S0 and Sext was covered in MD simulations. The amino acids sequence of the selectivity filter of potassium ion channels is conserved, with the exception that an isoleucine residue in eukaryotic potassium ion channels often is substituted with a valine residue in prokaryotic channels.[28]
Hydrophobic region[edit]
This region is used to neutralize the environment around the potassium ion so that it is not attracted to any charges. In turn, it speeds up the reaction.
Central cavity[edit]
A central pore, 10 Å wide, is located near the center of the transmembrane channel, where the energy barrier is highest for the transversing ion due to the hydrophobity of the channel wall. The water-filled cavity and the polar C-terminus of the pore helices ease the energetic barrier for the ion. Repulsion by preceding multiple potassium ions is thought to aid the throughput of the ions. The presence of the cavity can be understood intuitively as one of the channel's mechanisms for overcoming the dielectric barrier, or repulsion by the low-dielectric membrane, by keeping the K+ ion in a watery, high-dielectric environment.
Potassium channel blockers, such as 4-aminopyridine and 3,4-diaminopyridine, have been investigated for the treatment of conditions such as multiple sclerosis.[29]
These blockers work in a way to inhibit the flow of potassium ions through the KcsA channel. They either compete with potassium when binding to KcsA channel or they bind to the outside of the channel on an external binding site causing a conformational change, which closes the channel. An example of one of these competitors is quaternary ammonium ions, thought to be toxins that inhibit the binding of potassium.[30] In a study it was found that Tyr82 residues provides a good external binding site for blockers, especially the quaternary ammonium ions.[31]
Muscarinic potassium channel[edit]
See also G protein-coupled inwardly-rectifying potassium channel
Some types of potassium channels are activated by muscarinic receptors and these are called muscarinic potassium channels (IKACh). These channels are a heterotetramer composed of two GIRK1 and two GIRK4 subunits.[32][33] Examples are potassium channels in the heart, which, when activated by parasympathetic signals through M2 muscarinic receptors, cause an outward current of potassium, which slows down the heart rate.[34][35]
Potassium channels in fine art[edit]
Roderick MacKinnon commissioned Birth of an Idea, a 5-foot (1.5 m) tall sculpture based on the KcsA potassium channel.[36] The artwork contains a wire object representing the channel's interior with a blown glass object representing the main cavity of the channel structure.
See also[edit]
- ^ Littleton JT, Ganetzky B (2000). "Ion channels and synaptic organization: analysis of the Drosophila genome". Neuron 26 (1): 35–43. doi:10.1016/S0896-6273(00)81135-6. PMID 10798390.
- ^ Hille, Bertil (2001). "Chapter 5: Potassium Channels and Chloride Channels". Ion channels of excitable membranes. Sunderland, Mass: Sinauer. pp. 131–168. ISBN 0-87893-321-2.
- ^ Jessell, Thomas M.; Kandel, Eric R.]]; Schwartz, James H. (2000). "Chapter 6: Ion Channels". Principles of Neural Science (4th ed.). New York: McGraw-Hill. pp. 105–124. ISBN 0-8385-7701-6.
- ^ Rang, HP (2003). Pharmacology. Edinburgh: Churchill Livingstone. p. 60. ISBN 0-443-07145-4.
- ^ Kobayashi T, Washiyama K, Ikeda K (2006). "Inhibition of G protein-activated inwardly rectifying K+ channels by ifenprodil". Neuropsychopharmacology 31 (3): 516–24. doi:10.1038/sj.npp.1300844. PMID 16123769.
- ^ a b c d e f Enyedi P, Czirják G (2010). "Molecular background of leak K+ currents: two-pore domain potassium channels". Physiological Reviews 90 (2): 559–605. doi:10.1152/physrev.00029.2009. PMID 20393194.
- ^ a b c d e f Lotshaw DP (2007). "Biophysical, pharmacological, and functional characteristics of cloned and native mammalian two-pore domain K+ channels". Cell Biochemistry and Biophysics 47 (2): 209–56. doi:10.1007/s12013-007-0007-8. PMID 17652773.
- ^ Fink M, Lesage F, Duprat F, Heurteaux C, Reyes R, Fosset M, Lazdunski M (1998). "A neuronal two P domain K+ channel stimulated by arachidonic acid and polyunsaturated fatty acids". The EMBO Journal 17 (12): 3297–308. doi:10.1093/emboj/17.12.3297. PMC 1170668. PMID 9628867.
- ^ Goldstein SA, Bockenhauer D, O'Kelly I, Zilberberg N (2001). "Potassium leak channels and the KCNK family of two-P-domain subunits". Nature Reviews Neuroscience 2 (3): 175–84. doi:10.1038/35058574. PMID 11256078.
- ^ Sano Y, Inamura K, Miyake A, Mochizuki S, Kitada C, Yokoi H, Nozawa K, Okada H, Matsushime H, Furuichi K (2003). "A novel two-pore domain K+ channel, TRESK, is localized in the spinal cord". The Journal of Biological Chemistry 278 (30): 27406–12. doi:10.1074/jbc.M206810200. PMID 12754259.
- ^ Czirják G, Tóth ZE, Enyedi P (2004). "The two-pore domain K+ channel, TRESK, is activated by the cytoplasmic calcium signal through calcineurin". The Journal of Biological Chemistry 279 (18): 18550–8. doi:10.1074/jbc.M312229200. PMID 14981085.
- ^ Kindler CH, Yost CS, Gray AT (1999). "Local anesthetic inhibition of baseline potassium channels with two pore domains in tandem". Anesthesiology 90 (4): 1092–102. doi:10.1097/00000542-199904000-00024. PMID 10201682.
- ^ a b c Meadows HJ, Randall AD (2001). "Functional characterisation of human TASK-3, an acid-sensitive two-pore domain potassium channel". Neuropharmacology 40 (4): 551–9. doi:10.1016/S0028-3908(00)00189-1. PMID 11249964.
- ^ Kindler CH, Paul M, Zou H, Liu C, Winegar BD, Gray AT, Yost CS (2003). "Amide local anesthetics potently inhibit the human tandem pore domain background K+ channel TASK-2 (KCNK5)". Journal of Pharmacology and Experimental Therapeutics 306 (1): 84–92. doi:10.1124/jpet.103.049809. PMID 12660311.
- ^ Punke MA, Licher T, Pongs O, Friederich P (2003). "Inhibition of human TREK-1 channels by bupivacaine". Anesthesia & Analgesia 96 (6): 1665–73. doi:10.1213/01.ANE.0000062524.90936.1F. PMID 12760993.
- ^ Lesage F, Guillemare E, Fink M, Duprat F, Lazdunski M, Romey G, Barhanin J (1996). "TWIK-1, a ubiquitous human weakly inward rectifying K+ channel with a novel structure". The EMBO Journal 15 (5): 1004–11. PMC 449995. PMID 8605869.
- ^ Duprat F, Lesage F, Fink M, Reyes R, Heurteaux C, Lazdunski M (1997). "TASK, a human background K+ channel to sense external pH variations near physiological pH". The EMBO Journal 16 (17): 5464–71. doi:10.1093/emboj/16.17.5464. PMC 1170177. PMID 9312005.
- ^ Reyes R, Duprat F, Lesage F, Fink M, Salinas M, Farman N, Lazdunski M (1998). "Cloning and expression of a novel pH-sensitive two pore domain K+ channel from human kidney". The Journal of Biological Chemistry 273 (47): 30863–9. doi:10.1074/jbc.273.47.30863. PMID 9812978.
- ^ Meadows HJ, Benham CD, Cairns W, Gloger I, Jennings C, Medhurst AD, Murdock P, Chapman CG (2000). "Cloning, localisation and functional expression of the human orthologue of the TREK-1 potassium channel". Pflügers Archiv : European Journal of Physiology 439 (6): 714–22. doi:10.1007/s004240050997. PMID 10784345.
- ^ Patel AJ, Honoré E, Lesage F, Fink M, Romey G, Lazdunski M (1999). "Inhalational anesthetics activate two-pore-domain background K+ channels". Nature Neuroscience 2 (5): 422–6. doi:10.1038/8084. PMID 10321245.
- ^ Gray AT, Zhao BB, Kindler CH, Winegar BD, Mazurek MJ, Xu J, Chavez RA, Forsayeth JR, Yost CS (2000). "Volatile anesthetics activate the human tandem pore domain baseline K+ channel KCNK5". Anesthesiology 92 (6): 1722–30. doi:10.1097/00000542-200006000-00032. PMID 10839924.
- ^ Rogawski MA, Bazil CW (July 2008). "New Molecular Targets for Antiepileptic Drugs: α2δ, SV2A, and Kv7/KCNQ/M Potassium Channels". Curr Neurol Neurosci Rep 8 (4): 345–52. doi:10.1007/s11910-008-0053-7. PMC 2587091. PMID 18590620.
- ^ Doyle DA, Morais Cabral J, Pfuetzner RA, Kuo A, Gulbis JM, Cohen SL, Chait BT, MacKinnon R (1998). "The structure of the potassium channel: molecular basis of K+ conduction and selectivity". Science 280 (5360): 69–77. Bibcode:1998Sci...280...69D. doi:10.1126/science.280.5360.69. PMID 9525859.
- ^ MacKinnon R, Cohen SL, Kuo A, Lee A, Chait BT (1998). "Structural conservation in prokaryotic and eukaryotic potassium channels". Science 280 (5360): 106–9. Bibcode:1998Sci...280..106M. doi:10.1126/science.280.5360.106. PMID 9525854.
- ^ Armstrong C (1998). "The vision of the pore". Science 280 (5360): 56–7. doi:10.1126/science.280.5360.56. PMID 9556453.
- ^ "The Nobel Prize in Chemistry 2003". The Nobel Foundation. Retrieved 2007-11-16.
- ^ Zhou Y, Morais-Cabral JH, Kaufman A, MacKinnon R (2001). "Chemistry of ion coordination and hydration revealed by a K+ channel-Fab complex at 2.0 Â resolution". Nature 414 (6859): 43–8. doi:10.1038/35102009. PMID 11689936.
- ^ a b Hellgren M, Sandberg L, Edholm O (2006). "A comparison between two prokaryotic potassium channels (KirBac1.1 and KcsA) in a molecular dynamics (MD) simulation study". Biophys. Chem. 120 (1): 1–9. doi:10.1016/j.bpc.2005.10.002. PMID 16253415.
- ^ Judge SI, Bever CT (July 2006). "Potassium channel blockers in multiple sclerosis: neuronal Kv channels and effects of symptomatic treatment". Pharmacol. Ther. 111 (1): 224–59. doi:10.1016/j.pharmthera.2005.10.006. PMID 16472864.
- ^ Luzhkov, V.B.; J. Åqvist (14 February 2005). "Ions and blockers in potassium channels: insights from free energy simulations". Biochimica et Biophysica Acta (BBA) - Proteins & Proteomics 1747 (1): 109–120. doi:10.1016/j.bbapap.2004.10.006.
- ^ Luzhkov, Victor B.; Fredrik Osterberg, Johan Aqvist (26 September 2003). "Structure–activity relationship for extracellular block of K+ channels by tetraalkylammonium ions". FEBS Letter 554 (1–2): 159–164. doi:10.1016/S0014-5793(03)01117-7.
- ^ Krapivinsky G, Gordon EA, Wickman K, Velimirović B, Krapivinsky L, Clapham DE (1995). "The G-protein-gated atrial K+ channel IKACh is a heteromultimer of two inwardly rectifying K+-channel proteins". Nature 374 (6518): 135–41. Bibcode:1995Natur.374..135K. doi:10.1038/374135a0. PMID 7877685.
- ^ Corey S, Krapivinsky G, Krapivinsky L, Clapham DE (1998). "Number and stoichiometry of subunits in the native atrial G-protein-gated K+ channel, IKACh". J. Biol. Chem. 273 (9): 5271–8. doi:10.1074/jbc.273.9.5271. PMID 9478984.
- ^ Kunkel MT, Peralta EG (1995). "Identification of domains conferring G protein regulation on inward rectifier potassium channels". Cell 83 (3): 443–9. doi:10.1016/0092-8674(95)90122-1. PMID 8521474.
- ^ Wickman K, Krapivinsky G, Corey S, Kennedy M, Nemec J, Medina I, Clapham DE (1999). "Structure, G protein activation, and functional relevance of the cardiac G protein-gated K+ channel, IKACh". Ann. N. Y. Acad. Sci. 868 (1): 386–98. Bibcode:1999NYASA.868..386W. doi:10.1111/j.1749-6632.1999.tb11300.x. PMID 10414308.
- ^ Ball, Philip (March 2008). "The crucible: Art inspired by science should be more than just a pretty picture". Chemistry World 5 (3): 42–43. Retrieved 2009-01-12.
External links[edit]
- Proteopedia Potassium_channel in 3D
- Potassium Channels at the US National Library of Medicine Medical Subject Headings (MeSH)
- Neuromuscular Disease Center (2008-03-04). "Potassium Channels". Washington University in St. Louis. Retrieved 2008-03-10.
- UMich Orientation of Proteins in Membranes families/superfamily-8


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Tips to picking healthy dressing
A crisp, refreshing salad sounds like a healthy choice for those watching their weight, eating to nourish their body and those who have a true love affair with the greens we need. However, a simple salad can quickly go wrong if prepared with sneaky health impostor ingredients.
Salad dressing is the most common sabotaging salad ingredient. Whether you are dining at a salad bar or shopping at the grocery market, apply these salad dressing secrets to avoid health inhibiting ingredients so you can truly nourish your body.
Pick the right consistency
When at a restaurant or cafe choose, "clear and runny" dressings over "gloopy-gloppy" dressings. For example, an oil-based dressing, which is clear in consistency, is traditionally a healthier choice than a "gloopy-gloppy" dressing, which is traditionally thick, difficult to spread and dairy based, such as blue-cheese, ranch or thousand-island dressings. Also, don't be afraid to ask your server about the ingredients used in your dressing!
Light isn't always right
When grocery shopping, "light" or "lite" options do not always guarantee a healthier choice. Lighter varieties commonly contain artificial sweeteners such as aspartame or sucralose, and additional harmful ingredients to your health. Always read the ingredient list of any bottled or packaged item you are considering consuming, and avoid chemically created or altered ingredients such as aspartame and sucralose.
Approved salad dressing ingredients
Some basic ingredients that make the cut include lemon, lime, sea salt, pepper, spices, garlic, organic virgin olive oil and organic raw unrefined coconut oil.
Homemade salad dressings are also great and can simply be made by blending together a few fresh ingredients. Try my Creamy Avocado and Zesty Lime Salad Dressing!
Say no to canola oil
Olive oil comes from olives, peanut oil comes from peanuts and canola oil comes from, rapeseeds? Did you know that there is no such thing as the "canola nut"? Rapeseed oil was originally produced in the 19th century as a source of lubricant for steam engines. It is also important to note that most canola, 93 percent in the U.S. to be exact, is genetically modified. Avoid salad dressings containing canola oil. Instead choose salad dressing made with organic virgin olive oil or organic raw unrefined coconut oil.
... and corn syrup
High Fructose Corn Syrup (HFCS) is a common ingredient found in commercial salad dressing. It is added to sweeten up your dressing, while reducing the overall cost. However this additive does have a cost—your health! HFCS is difficult for your body to metabolize and has been linked to many health problems such as obesity and diabetes. Avoid any salad dressing that contains this health-inhibiting ingredient.
Creamy Avocado and Zesty Lime Salad Dressing
Yields 1 cup or 16 tablespoons
More salad recipes
Summer nectarine salad with fresh basil dressing
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All too many people think that electricity comes out of two holes in the wall. Few people realize that about half of the nation's electricity is generated in coal-fired power plants. Still fewer realize that the United States is the world's largest generator of electricity from nuclear power plants. Although Colorado generated electricity from nuclear energy for about thirteen years, that plant now generates electricity with natural gas to create the steam.
Coal- Colorado gets most of its electricity from coal-powered plants and, of necessity, will continue to do so for a long time into the future. Fortunately, Colorado has an abundant supply of clean coal.
Natural gas- Natural gas is the second leading fuel source for power plants in Colorado. It is considered to be a cleaner-burning fuel and has been increasing in use throughout the United States. Colorado is fortunate to have an abundant supply of natural gas. Indeed, we have the 7th largest natural gas field in the United States just north of Denver.
Nuclear- Colorado had a short-lived experience with nuclear-fueled, electric generation. The Fort Saint Vrain nuclear power plant near Platteville was built in the 1970s. This was an experimental type of facility and proved to be so expensive and problem plagued that after 13 years of operation it was converted to a natural-gas-powered plant. Unless the nation as a whole decides to return to nuclear-fueled power plants, it is unlikely that this fuel source will be a factor in Colorado electricity generation.
Renewables- In 2004, the voters of Colorado passed a Renewable Energy initiative, the first-ever statewide initiative in the country. It requires that 10% of our electricity be generated from renewable sources by 2015. Renewable energy resources include solar, wind, geothermal, biomass, small hydroelectricity, and hydrogen fuel cells.
Wind presently generates only 0.2% of our electricity. However, new wind farms are springing up in many places. The technology of wind generators has improved considerably over the past two decades. It is likely that much of the required new sources in the initiative will be from wind.
Dams generate 3% of our electricity. Today, it is extremely difficult to build new dams in the state. Therefore, it will be difficult to realize much growth in this power source.
Presently, solar energy is predominantly used for generating electricity onsite for electronic instruments in remote locations. This technology has advanced significantly, but is still quite expensive. However, entire houses in Colorado are now powered completely by solar energy. The technology will continue to advance and prices will continue to come down.
The Solar Electric Power Association ranks Xcel Energy, Colorado's largest energy supplier, as the 8th largest solar power producer in the USA based on Megawatts of capacity.
The association ranks Colorado among the top 7 states for potential solar power generation. The table shows solar potential, not actual constructed capacity. Colorado covers 104,094 square miles, with 2,124 square miles regarded as having high potential for solar power generation. This represents 2.04% of the total surface area of the state.
Solar Potential From Very Large Scale Solar Power Plants:
Land Used
(sq miles)
Annual Generation


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October 6, 2011
Nonsensical Infographics
We posted about Chad Hagen a couple years ago, but I recently stumbled upon some of his new work and think that it is definitely worthy of a second post. These Nonsensical Infographics are fun and beautiful and I would love to have one to hang over my desk.
Check out more below the jump!
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Each event is unique as all 6 games have their own gestures that assist you while playing. Each event promises a highly-detailed and interactive experience as your every movement with the Move controller changes the movement of your on-screen character.
Each game offers different locations where the event takes places adding versatility to Sports Champions, though the gameplay remains the same. For example, Bocce offers different courts on which you can play the game, while there are 18 different holes in disc golf. The movements are smooth and there is no noticeable delay between your movement and the movement of the character on screen.
Developed by San Diego Studio and Zindagi Games and published by Sony Computer Entertainment, Sports Champions is such a game that provides entertainment and fitness to the whole family. The Move controller is required to play all the games as it tracks your movements and matches them with the game elements. The controller adds in more involvement in the game as it can measure even the slightest wrist movements and adjust the trajectory as needed.
The game has 3 gameplay modes that are named as Free Play, Challenge Mode and Champion Cup mode. Free Play allows you to practice all the games, any time you want. This mode assists you to improve your gameplay as you can practice any game without losing.
In Challenge Mode you compete in a series of events to improve your scores. This is a little more challenging than the Free Play mode as with each loss you lose points. In Champion Cup mode, you play against 10 other athletes in an event that is similar to Olympics to win the cup and become the ultimate champion. 4 players can play at the same time in Sports Champions. You can select various modes and challenge your friends and duel against them for a win, improving your scores each time.
The game allows the wielding of 2 Move controllers by a single player. This allows you to improve your aim in games like Archery and more. You can use one controller as a bow and equip it with an arrow using the other controller or you can use one controller as a sword and the other as a shield, depending upon the game.
Online Features
You can compare stats, experiences and everything related to the game through an online leader board. By keeping track of the high scores and other things, you can keep track of the high-scorers and improve your own scores to reach the top. The rank board varies from novices to the best players of all-time. The PSN network allows you to connect and download updates, if any, and many other things that make playing the game a wholesome experience.
Buying Guide
A minimum distance of 6 ft is required between the player and PS3 console camera for smooth game play. More space is required if extra players join in. Try to place the gaming console in a living room or the main hall to provide freedom for your hand and leg gestures. Ensure that the room has proper and even lighting; this helps the camera to capture your every moment and give you a seamless and entertaining gaming experience.
|Sports Champions (Move Required)
|Sony Computer Entertainment
While We always wished a Game Which we could play on our own , by real movements not a controller , Sony , Microsoft , Nintendo Made That Dream True By Launching Kinect or Move ,etc But When It Comes To What is Better Then Move Was the winner With The Titles Fight . Sports Champion Is a reason why move is the best . With Games Like Table Tennis , Volley Ball , Disc Golf and the others are great . Its a Great Exercise Partner For PS3 and Move Owners . Though Remember You Will Need Minimum 1 ( Better If 2 But Not Necessary ) PlayStation Move Motion Controller and PlayStation Eye Camera To Play This Game . It won't Work With A PlayStation Navigation Controller , Sony DualShock 3 Gamepad , Or any Other Gamepad . If You Have What are you Waiting For Go for it .
Thanks a lot flipkart ! delivered within 2 days of ordering (at morning)
perfectly packed and a very good price!
all the game are good ,specially table tennis (will have to buy one more controller to play all the games like gladiator).
overall a game worth buying.
Couldnt find it in any other shop (tried landmark,jumbo,and other stores)
thanks again flipkart.
1. Good Value for money. You get 5 sports games in one CD.
2. The game surprises you at each level.( Go play it for yourself and figure out. I don't want to give out the spoilers here :-) ).
3. Some games like Archery & Beach Volleyball work pretty well with just a single Move controller too even though the game says you need 2 controllers for best experience.
4. Playing one game of Gladiator Duel is like working out in the gym for 30 minutes. It leaves you exhausted!
1. You cannot customize the character that you choose.
2. When you win a 3 Star Victory in the Champions Cup, it says: You have won the Opponent's costume for that Cup. But you never see your player wearing that costume in the next round. It also says you have won some objects but I am yet to figure out how to make the player start using those objects.
3. Games like Bocce do get monotonous if you are playing with the CPU.
yes it is totally fantastic game for those who needs wok out at home without playing real life games such as table tennis,archary,volleyball etc specially gladiater combat i like it very much...........good graphics, but it needs motion controller for playing such games.....................but the bad points is after playing for a short time u feel hactic....so dont play continously take a break after few minutes of play....
There are 6 games in this disc: Archery, Beach Volleyball, Table Tennis, Gladiator Duel, Disc Golf & Bocce!
The program can take you through how-to sessions of basic game play or you can proceed to play directly.
Play as a single player or up-to four players can play simultaneously (provided you have four move controllers).
Games like Archery and Gladiator Duel require two move controllers per person for effective gaming.
Overall, a good starting point for people to get to know and use their Move controllers; most of my friends started their PS3 Move experience with this disc.
Note: When you buy the PS3 Move Starter Pack, you can try out the included Sports Champions game demo before buying the full version.
The various games on the disc make for a very enjoyable evening. I found that the games (except Table Tennis) were pretty easy...Read More
All the games are just great but the best among is disc golf
I recommend everyone to buy it and is fun to play mu...
This was my first game. I enjoyed a lot esp Table tennis and archery.Movements are good and did not had any problem while playi...Read More
Flipkart didnt rock this time . Flipkart delivered it to me in 7-8 days.
Now this game is the best ps move game of all t...
superb game
in this game we can play with our own hands this game can be compared by wii sports or kinect season 1 this...


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Home > Interconnections > Sockets and Pins
Helpful tips for the early engineer or hobbyist
While "no soldering required" and "simplifying soldering" have both been used as selling points for many different products, sooner or later, you're going to have to heat the iron and get down to business.
Here are some quick tips for safe soldering and desoldering when necessary.
Selecting Your Solder. Make sure to note whether the solder you're working with contains lead — if it does, make sure to wash your hands regularly to avoid absorbing it. (Another option is lead-free solder, but that comes with its own questions .)
Catching Your Breath. Soldering produces fumes, and you don't want to breathe them in. Ensure that your workspace is well ventilated, and if you plan to be soldering for a long period of time, work with an exhaust fan when possible.
Protecting Your Eyes. A lot of people skip protective eyewear, but safety goggles are an important part of any safe workspace. Spatter may be rare, but it's always better to be safe than sorry.
Keeping Your Cool.Never forget that your soldering iron is hot! Once you've preheated the iron, make sure that you only hold it by the insulated grip, and always return it to its stand after you've used it.
Fixing Your Mistakes. Soldering isn't permanent! In fact, just as soon as you start soldering, you'll likely want to start desoldering . If you decide to use desoldering wick, remember that it is made of copper and it will get very hot.
Keep Your Iron Clean. A clean iron tip means better heat conduction. Use a damp sponge to wipe the still-hot soldering iron between uses.
Do you have any burning questions about soldering? Post your ideas and questions on the TechXchange forum . ■
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I wonder if a winning streak or desire to get to .500 through this kind of bonding and or motivation is replicated in the WNBA on a different level.
Bearded Mavericks invite barber to attend Thursday's break-even game
By Rob Mahoney
A good chunk of the Mavericks roster bonded via bearded solidarity this season, collectively vowing in early February to continue growing out their facial until the team registered a .500 record. That's a relatively low benchmark for a franchise that has made the playoffs in each of the last 12 seasons, but an injury to Dirk Nowitzki and an incredible amount of roster turnover forced Dallas to reset its standards. An even record became the new goal, and until that goal was reached, the faces of select Mavs would only grow woolier and woolier.
Not all of the Mavs have played by the rules of their beard pact, but Nowitzki stands as a beacon of the team's hopes, insofar as any shaggy chin ever could. Deadspin's Barry Petchesky chronicled the evolution of Nowitzki's beard in photo form, though his tribute may wind up as something of a eulogy.
With Tuesday's win over the the Clippers — and 13 wins over a 20-game stretch — Dallas is now 35-36 overall with an eye toward Thursday's matchup with the Pacers, which provides a chance to break even. Nowitzki, in particular, seems eager to shed his soup-catcher — so much so that the Mavs have invited a hand-picked barber to attend Thursday's game in the hopes of trimming down postgame. Eddie Sefko of the Dallas Morning News has the scoop:
"Everyone will have the clippers in the locker room Thursday," Mayo said after the Mavericks' robust 109-102 overtime win over the Clippers Tuesday. "Hopefully guys can watch us shave it off. The barber will be here. We'll leave him tickets (for the game) and hopefully give ourselves a chance to shave it off. I want to do it right. I don't want any patches. I'm ready to shave it."
Apparently, Omar the barber is going to do the honors. No clear word on who's barber Omar is, but he'll certainly be a popular guy Thursday night if the Mavericks can pull off their fourth consecutive victory.
Nowitzki didn't really want to talk about the possibilities, preferring not to open the Mavericks up to any voodoo that might befall them if they take anything for granted.
"I don't really want to jinx it, but I'm ready to get this thing off," he said. "That's a big outing for us Thursday against a very good, tough team from the Eastern Conference."
Unfortunately for Dirk and the few Mavs that have continued to grow out their beards, Thursday's game is hardly a lock. The Pacers are one of the toughest teams on Dallas' remaining schedule, and subsequent games agains the Bulls, Lakers and Nuggets will offer no chance for a quick and easy rebound. Late-season affairs against Portland, Phoenix and New Orleans should give the Mavs a few more chances to hit .500, but the barber's presence Thursday should up the stakes in a game that's already significant thanks to Dallas' impressive playoff chase.


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1. Follow Route 1 North/Crystal City
2. Take the 15th Street/Pentagon City exit
3. Turn left onto 15th Street
4. Travel three blocks
5. Turn right onto South Hayes Street
6. The Ritz-Carlton, Pentagon City luxury hotel is located on the left, adjacent to Nordstrom
1. Follow I-66 East
2. Take Exit 75 (Route 110 South)
3. Continue past the Pentagon
4. Take the exit marked Route 1 South (Crystal City)
5. Take the 15th Street/ Pentagon City exit
6. Turn right onto 15th Street and continue three blocks
7. Turn right onto South Hayes Street
8. The Ritz-Carlton, Pentagon City in Arlington, VA, is located on the left, adjacent to Nordstrom near the metro
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Larry Bird finished his outstanding NBA career in 1992, with averages of more than 24 points, 10 rebounds and 6 assists per game in his final season. Following Bird's departure, the Celtics promptly retired his jersey number 33. Now is your chance to wear the jersey of a Celtics legend with this 1992 Larry Bird Authentic jersey by Mitchell & Ness! Reproduced in perfect detail, Mitchell & Ness pays close attention while designing each individual piece, in an attempt to re-create each jersey exactly as it was back in the day.
- Felt tag with player name and year sewn-on above jock tag
- Heavyweight mesh body
- Tackle twill numbers & lettering
- Rib-knit collar & arm holes
- Embroidered NBA logo
- Jock tag
- Side slits at hem
- Imported
- 100% Polyester fabric
- Officially licensed NBA product
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Special event items are produced by manufacturers only after the outcome of a game or event. These are advanced sale items and will ship immediately after they are received in our warehouse.
Manufacturer direct items are shipped directly from the manufacturer. These items are not available for international or expedited shipping.
Customized items can be personalized with options such as your name, your favorite number, and/or designs. Some options may be limited by league rules.


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Compañía Cervecera de Canarias has given more than 5.300 boxes of Appletiser to food banks in the Community
7 July 2009
- The Food Banks distributes the donated product among 220 charity organizations
that reach more over 45 thousand users in the whole Archipelago.
- The company collaborates with other non-governmental that work with the most unprivileged groups of the Canarian society.
Santa Cruz de Tenerife, July 3, 2009.- Compañía Cervecera de Canarias has given 127.474 units of Appletiser to the Food Banks of Canary Islands. The donated product is a 100% natural beverage, apple juice based, with no preservatives, a well accepted product in Canary Islands and plenty European countries.
The current economic context has caused an increase in the food product demand on behalf of the non-governmental organizations of the Archipelago. Compañía Cervecera de Canarias has responded to this call and has widen the usual collaboration with this type of institutions, making an extraordinary delivery to the Food Banks of Canary Islands of 127.474 units of one of its star products, Appletiser, a 100% natural beverage.
The Food Banks distribute the donated products to other charity and social service institutions to be distributed among their beneficiaries. In the case of the Canary islands, they work with 220 organizations that reach 45.034 users in the whole Archipelago.
The company, which is very loyal to its commitment to the sustainable development with the Islands, usually collaborates with different non-governmental organizations dedicated to help the most unprivileged groups of the society such as: Aldeas Infantiles, Cáritas, UNICEF, Asociación Corazón y Vida, Hermanos de la Cruz Blanca, Hospital San Juan de Dios, SINPROMI, or the Asociación Regional de Parkinson de las Islas Canarias, among others.
For Luis Durango, responsible of Corporative Communication of the company: "Our role in social matter not only carries out charity contributions, but also we are involved in other matters that we know are important for Canary Islands, in those that we think we can be useful."
About Compañía Cervecera de Canarias
CCC is one of the main beer producer company at national level and one of the main motors of the economic, industrial and social development of the Canary Islands. It has over 300 Canarian entrepreneurs among their shareholders, as well as they are part of the SABMiller international group.
Compañía Cervecera de Canarias is placed among the main wealth and economic development generator Canarian companies of the Archipelago, boosting the creation of 900 direct jobs and more than 13.000 indirect jobs.
About Appletiser
Appletiser is a refreshing and distinct beverage made 100% apple juice, of selected varieties (Granny Smith, Starking, Golden Delicious and Royal Gala), slightly sparkling, no artificial colors, no preservatives, no sugar added, widely accepted in the Canarian market since 1969.
About the Food Banks
The Food Banks are nonprofit organizations based on volunteering, which goal is to recover the food surplus of our society and redistribute among people in need, avoiding any waste or misuse. Their saying is: "We need what you have plenty of."
This SABMiller subsidiary news release has been translated from its local market language to English language for publication on www.sabmiller.com. We have attempted to provide an accurate translation of the original material but due to the difficulties of translation slight differences may exist.
Note, the news release was first published in its local market on 03-06-09.


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A new Wisconsin Historical Society website is coming mid-May 2014! See a preview >>
Definition: A civil town in Clark Co. at latitude 443837N and longitude 0903007W, created 24 Feb. 1873.
38 records found
Yahara River Parkway (HIstoric Marker Erected 1996
Yahara River, Dane Co.
Yankees in Wisconsin
yard (maritime)
yard (railroads)
Yarnell, Sawyer Co.
Yawkey, Cyrus Carpenter 1862 - 1943
yawl (maritime)
Yellow Banks
yellow dogs
Yellow Lake, Burnett Co.
Yellow River (Historic Marker Erected 1968)
Yellow River, Town of, Burnett Co.
Yellow-dog contracts
Yellowlake [origin of place name]
Yellowstone, Election precinct of, Iowa Co.
Yellowstone, Lafayette Co.
York Center, Dane Co.
York Island [origin of place name]
York Township [origin of place name]
York, Dwight A. 1939
York, Jackson Co.
York, Stanley 1931
York, Town of, Clark Co.
York, Town of, Dane Co.
York, Town of, Green Co.
York, Town of, Sauk Co.
Yorkville, Racine Co.
Yorkville, Town of, Racine Co.
You-know (logging)
Youmans, Henry Mott 1851 - 1931
Youmans, Theodora Winton, 1863 - 1932
Young America, Washington Co.
Young, Leon D. 1967
Young, Rebecca 1934
Yuba [origin of place name]
Yuba, Richland Co.
Yuba, Village of, Richland Co.


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By creating an account with our store, you will be able to move through the checkout process faster, store multiple shipping addresses, view and track your orders in your account and more.
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Good Day Atlanta's Tacoma Perry not only enjoyed a great front row seat for the Peachtree Road Race, but also a fun look at this year's official, coveted event T-shirt.The T's are black this year, which some people are saying is an interesting choice for a commonly white T-shirt. But, runners – on foot and in wheelchairs – all seemed to like it a lot.One happy runner was kind enough to share his shirt with Tacoma!CLICK ON THE VIDEO PLAYER ABOVE TO SEE THIS RULL REPORT!
WHBQ-TV | Fox 13 485 S. Highland St.Memphis, TN 38111Main Station: (901) 320-1313Newsroom: (901) 320-1340


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Test, test and retest. All our products are vetted in the real world using the live or die criteria of direct response. If it doesn't make margin day one, it's back to the drawing board.
Chances are your customers have already heard of our product before it hits your shelf. Through national television, radio and print, we spend millions every year to achieve multi-million impressions on our brands.
We're not a vanilla factory. Our products surprise and delight defying the conventions of both popular and tired categories to bring something truly special to your customers.
It's one thing to identify your target audience. It's another thing to get them to sing your praises. Every one of our products has a phonebook-thick database of customers willing to tout its triumphs.
We recognize the most important ingredient in a product's launch is the retailer themselves. Without the right partnership, even the greatest product doesn't stand a chance. We consider our retailers strategic allies, and strive for mutual benefit every step of the way.
Knowing your market. Knowing your costs. Knowing that if you knock, somebody's home and they're salivating for your product. We don't believe there's one thing that guarantees retail success. We believe there are five. At martFIVE™ we've built a product development engine based on FIVE powerful principles that give us an unfair advantage in launching products through retail. Nothing is left to chance. We prove it, so you can move it.
Email email@example.com if you are interested in learning how you can become an exclusive retailer for HurryCane™ or Stuffies™, and how you can carry inventory risk-free.
Register online, if you like to secure your exclusive relationship with HurryCane™ and Stuffies™ right now.
Reorder here, if you are a Returning Partner.


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1 cup black quinoa
2 medium oval sweet potatoes
1 pomegranate
1/2 chopped red onion
3/4 cup chopped pecans
Sea salt and black pepper to taste
½ teaspoon nutmeg
1 tsp coconut oil
1 tsp honey to drizzle
4 green olives
1 green pepper cut into thin slices
Preheat oven to 375 degrees
Wash and scrub sweet potatoes and prick with a fork
Bake sweet potatoes on pan for about 40-50 mins or until tender
While sweet potatoes are baking, cook quinoa to package instructions
After quinoa is finished cooking, combine onions, pecans, nutmeg, and pomegranate seeds to quinoa and stir
Allow sweet potatoes to cool slightly and cut in half longwise
Fill each sweet potato half with 1/4 quinoa mixture
Decorate each "coffin" with green olive head and green peppers for body
Drizzle each coffin with honey if desired.
Halloween Freezer Bark
1 cup almond butter
3 tbsp coconut oil
1/2 tsp salt
1 and 1/2 tbsp maple syrup
1/2 cup of Sunspire chocolate pieces
Combine almond butter, coconut oil, salt, and maple syrup and stir well. Place mixture in a 8x8 pan or small dish lined with parchment paper
Top with chocolate pieces
Place in freezer for at least 3 hours


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Ray Emery is quite the troubled soul these days. His tirade at the end of Thursday's pre-game skate followed by a lame excuse for being late to Friday's practice was, to put it lightly, very childish. The fact that Senators head coach John Paddock sent him home from the rink sulking like a disappointed pre-teen schoolgirl instead of a pro hockey player is just another nail in his coffin. The organization has simply had enough of Emery's absurd antics and if he isn't careful he'll go right off the deep end into NHL anonymity.
Call it a distraction, call it flamboyant over-zealousness. Whatever it is, it's not making his teammates very happy. The stories are stacking up like something out of that horrible TMZ show – everything from his road rage to his wardrobe to his recent noticeable and ludicrous lack of effort at practice, there's always a story with 'Rageaholic Ray'. Nobody wants to hear a pro hockey player whine, and even though Emery may not be verbally whining, he is certainly showing ridiculous immaturity through his actions.
To his credit, he did respond to Friday's fiasco by showing up to practice early on Saturday morning in order to work with goalie coach Eli Wilson. While that may have calmed the stormy seas just a little bit, rest assured the media buzz heading into Saturday night's game against the Washington Capitals was still focused on Emery's attitude problems as opposed to Martin Gerber continuing his great play or how to contain Alex Ovechkin. Having the reputation of a goalie with on and off-ice problems is the worst thing that can possibly happen. You're nothing but a nuisance, a scab that won't heal, a festering wound.
In Emery's defense, there's a valid reason why he's been so visibly upset this season. It is said that no goalie should ever lose his starting job due to an injury, yet that's exactly what has happened. That would tear up any goalie inside and out, no matter what kind of mental framework the player has. Part of his frustration comes from his inability to perform at last year's level, as Emery is only 5-3-3 with an 89.1 save percentage and a mediocre 2.88 goals-against average this season. He started the season 2-0 with big wins over Florida and Atlanta but dropped his next three decisions to Washington, Buffalo and Philadelphia. Those three losses were key chances to win key games for his team, yet he was unable to perform. In 12 games, Emery has allowed four goals in five of them…not very starter-like. It's a frustrating time when capable goalies cannot come through for their teammates, so his unhappiness is a normal reaction - thrashing about and swinging a stick around at the end of a practice is not.
Obviously Martin Gerber's incredible and unexpected play this season coincided with Emery's injuries and inconsistency, making it virtually impossible to bench Gerber for anything more than two games. The Swiss goaltender is now 19-6-1 with a 2.50 goals-against average and a 92.0 save percentage. Since being pulled on December 1st against the Rangers after allowing three goals on 12 shots, Gerber has gone 6-2-0 and didn't allow more than three goals in any game until Saturday's 8-6 loss to the Capitals.
Speaking of Saturday's high-scoring affair, you can read a lot into the Emery debacle through coach Paddock's actions, or lack thereof. His decision not to pull Gerber after allowing Daniel Alfredsson's shorthanded goal halfway through the 2nd period could easily be seen as a disciplinary action against Emery. And when things went from bad to terrible after Nicklas Backstrom scored with three seconds remaining in the period, making the score 5-2, Emery sill remained on the bench. In any other situation there would have certainly been a goalie change to start the third.
Beyond the loss to the Capitals, it's honestly more that Emery's recent benching is a result of cause and effect more than a bad attitude. He's inconsistent and Gerber is playing stellar hockey. And whether it's due to the injuries or a wretched character, Emery is just not playing the same as last year. Sure, he may believe he deserves a chance to take back the starting status, but we all know it's not what he did for the Senators last year, but what he is doing right now. "What have you done for me lately?" is thrown around all the time, so he's handling the situation in the worst possible way – stick tirades and tardiness is flat out immaturity and selfishness.
Overall, Emery's current lack of a work ethic is like a mental sickness that can cause career suicide. Not only can he feel it internally, but he knows it's happening and that it's noticed by other players and teams, yet he has to play through it anyways. It can also possibly infect other players, so the only thing that can be done to stop the spread of this "sickness" is to quarantine him – or eliminate him.
Like quicksand, once you start sinking, the more you'll struggle and the further down you'll go. The best thing for Emery to do at this point is to put up and shut up by working hard and being patient while waiting for an imminent opportunity. Fantasy hockey managers are well advised to drop him like a ton of bricks and never look back.
Comment on Ray Emery and read Goldman's Blog here...
Read Dobber's Take on Ray Emery here...


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Klaus Strebel, Ph.D.Building 4, Room 3124 Memorial DriveBethesda, MD 20892-0460Phone: 301-496-3132Fax: email@example.com
Klaus Strebel received his Ph.D. in microbiology in 1985 from the University of Heidelberg, Germany. He joined the NIAID Laboratory of Molecular Microbiology (LMM) in 1986 as a postdoctoral fellow and is now head of the Viral Biochemistry Section within LMM.
Primate immunodeficiency viruses, including HIV-1, are characterized by the presence of a number of viral accessory genes that encompass vif, vpr, vpx, vpu, and nef. The vif, vpr, and nef genes are expressed in most HIV-1, HIV-2, and SIV isolates. In contrast, the vpu gene is found exclusively in HIV-1 and one SIV isolate, SIVcpz. The vpx gene, on the other hand, is not found in HIV-1 isolates but is common to HIV-2 and most SIV isolates. Defects in accessory genes are frequently not correlated with a detectable impairment of virus replication in continuous cell lines, in contrast to primary cell types, which more closely reflect the in vivo situation. The molecular basis for this cell-type-specific role of some of the accessory proteins remains largely unknown. However, it becomes increasingly clear that these proteins indeed exert important functions in their relevant target cells in vivo and, in fact, most if not all of the HIV accessory proteins exert multiple independent functions. The precise biochemical activity for most of the accessory proteins is currently not well understood; however, there is increasing evidence to suggest that they do not have catalytic activity on their own but rather function as adaptor molecules that connect other viral or cellular factors to various cellular pathways.
The primary objective of the section is to investigate the biological and biochemical functions of HIV accessory proteins, in particular Vif and Vpu, and to define their role in virus replication. This includes both the detailed biological and biochemical characterization of the individual viral proteins as well as the investigation of their engagement with distinct host factors. Understanding the molecular mechanisms of viral proteins will benefit our general understanding of the HIV replication process and may reveal new targets for antiviral therapy. In addition, the investigation of virus-host interactions will give us new insights into general cellular processes involved in protein trafficking, degradation, post-translational modification, and so forth.
The HIV-Accessory Protein VpuParallel with the discovery of vpu as a functional gene in 1987, we realized that its gene product, an 81-residue integral membrane protein, had an important function in regulating virus release (Strebel, 1989). These early studies were soon complemented by the realization that Vpu had a second, independent function during virus replication that resulted in the rapid degradation of CD4 receptor molecules from the endoplasmic reticulum in HIV-infected cells (Willey, 1992). One of the main goals of our subsequent research was to understand the molecular mechanisms involved in Vpu-mediated virus release and CD4 degradation. We found that CD4 degradation required a specific interaction of Vpu with newly synthesized CD4 molecules in the endoplasmic reticulum (Bour, 1995). This interaction was dependent on sequences in the cytoplasmic domains of CD4 and Vpu. The interaction of Vpu and CD4 was found to trigger a process that resulted in the rapid degradation of CD4. Using a yeast-two-hybrid-based screening of human cDNA libraries, we identified, in collaboration with Richard Benarous and his group at the Institute Cochin, France, a novel Vpu-binding protein, human-bTrCP (h-bTrCP), which functions as a ubiquitin ligase and connects CD4 to the proteolytic machinery (Margottin, 1998). Two essential structural motifs were identified in h-bTrCP: a C-terminal domain composed of seven WD repeats that is important for protein-protein interactions and an F-box motif located at the N-terminus that is functional in mediating interactions with Skp1, a protein recently identified as a targeting factor for ubiquitin-mediated proteolysis. We were able to show both in vivo and in vitro that the WD repeats mediate binding to Vpu (Margottin 1998). Interestingly, we found that h-bTrCP interacts with Vpu only when the latter is phosphorylated at serine 52 and 56, providing the first explanation as to why these highly conserved residues in Vpu are of crucial importance for CD4 degradation. The F-box of h-bTrCP, on the other hand, was found to mediate interactions with Skp1.
Figure 1: Vpu-induced degradation of CD4 involves TrCP (view enlarged illustration)Vpu can bind to newly synthesized CD4 in the endoplasmic reticulum. In addition, Vpu has a binding domain for TrCP. This domain includes two conserved serine residues in the cytoplasmic domain of Vpu that are constitutively phosphorylated by casein kinase 2 (CK-2). Formation of multiprotein complexes consisting of TrCP, Vpu, and CD4 results in the TrCP-dependent ubiquitination of CD4 and subsequent degradation by cytosolic proteasomes.
Based on our observation that Vpu inhibits TrCP-dependent degradation of IkB and thus blocked NF-kB activation (Bour, 2001), we explored the possible involvement of Vpu in HIV-1-induced apoptosis (Akari, 2001). We found that in HIV-1-infected CD4+ T cell lines as well as primary CD4+ T cells, expression of Vpu significantly contributed to the induction of apoptosis. Using an inducible expression system we found that the effect of Vpu on apoptosis was direct and did not require the co-expression of other viral proteins. Analysis of cellular factors involved in the induction of apoptosis demonstrated that Vpu down-modulated the NF-kB-dependent expression of anti-apoptotic genes such as Bcl-xL and A1/Bfl-1. Concomitantly, Vpu expression resulted in increased levels of active caspase-3. These effects of Vpu involved an interaction with TrCP as evidenced by the fact that mutation of the TrCP binding motif in Vpu abolished its apoptogenic potential. These results suggest that Vpu promotes apoptosis through its inhibition of NF-kB.
Figure 2: Mechanism of Vpu-induced apoptosis. (view enlarged image)In unstimulated cells, NF-kB resides in the cytoplasm in an inactive complex with its inhibitor IkB. Upon stimulation of cells by cytokines such as TNF-a (1), IkB is rapidly phosphorylated by an IkB specific kinase (2), which results in the rapid degradation of IkB via a TrCP-dependent pathway (3). Infection of cells by HIV-1 results in the gradual intracellular accumulation of Vpu. Because of its constitutively active TrCP-binding motif and the fact that it is not sensitive to TrCP-mediated proteolysis, Vpu functions as a competitive inhibitor of TrCP. This results in the gradual accumulation of IkB and the progressive impairment of the cell's ability to activate NF-kB (4). The inhibition of NF-kB blocks the synthesis of anti-apoptotic proteins such as the Bcl-2 family proteins (e.g., Bcl-xL and A1/Bfl-1) or TNFR complex proteins (e.g., TRAF1) (5). TRAF1 is induced by TNF-a treatment and normally inhibits activation of caspase-8 (6). In Vpu-expressing cells, the levels of TRAF1, in response to TNF stimulation, are reduced and no longer sufficient to inhibit the cytokine-induced activation of caspase-8 (6). Activated caspase-8 in turn induces the release of cytochrome c from the mitochondria (7). Release of cytochrome c is normally inhibited by the Bcl-2 family of proteins. However, in Vpu-expressing cells the levels of Bcl-2 proteins are limiting and no longer sufficient to block cytochrome c release (8). After its release from the mitochondria, cytochrome c forms ternary complexes with Apaf-1 and caspase-9 (9), resulting in the activation of caspase-3 (10). Active caspase-3 finally triggers a reaction that results in the cleavage of a number of target proteins including Bcl-2 family proteins (11) and leads to cell death (12).
The HIV-Accessory Protein VifThe HIV-1 Vif protein plays an important role in regulating virus infectivity (18). The lack of a functional Vif protein results in the production of virions with reduced or abolished infectivity (Strebel, 1987). This effect of Vif on virus infectivity is producer cell dependent and can vary by several orders of magnitude. Virus replication in non-permissive cell types such as H9 is strictly dependent on Vif, while Vif-defective viruses can efficiently replicate in permissive hosts such as Jurkat cells. The cellular factors determining the requirement for Vif are currently not known. Results from heterokaryon analyses, which involved the fusion of restrictive with permissive cell types suggested the presence of an inhibitory factor in restrictive cell types. However, the identity of the proposed inhibitory factor and its mode of action remain elusive. Recent work investigating the ability of Vif from different lentiviruses for cross-species trans-complementation suggested that Vif itself functions in a host-cell dependent manner, supporting the notion that Vif may interact with as yet unknown cellular factors.
Although vif genes are present in all lentiviruses, with the exception of equine infectious anemia virus, there is relatively little sequence conservation between different Vif variants. Nevertheless, HIV-1 Vif was found to be capable of functionally complementing Vif-defective HIV-2 and SIVmac isolates, suggesting common functional domains and a common mode of action. Similarly, HIV-2 Vif was capable of complementing HIV-1 Vif defects.
HIV-1 Vif associates with the intermediate filament vimentinA significant amount of Vif can be found in association with the intermediate filament network in virus-producing cells (Karczewski, 1996); however, the domain(s) in Vif responsible for this association as well as its functional significance remain to be determined.
Figure 3: Colocalization of Vif with the intermediate filament vimentin.HeLa cells were transfected with the Vif expression vector pNL-A1. To better visualize colocalization of Vif with vimentin, cells were treated with demecolcine (0.1 mg/ml) for 15 hours following transfection. Demecolcine treatment of HeLa cells results in a structural reorganization of vimentin intermediate filaments to form a nuclear cage structure. Cells were stained for vimentin (green) and Vif (red) Colocalization of Vif and vimentin is apparent by the yellow color. A Nomarski bright field image is shown in the right panel.
HIV-1 Vif is packaged into the nucleoprotein complex through an interaction with viral genomic RNADespite the severe impact of Vif defects on virus infectivity, its mechanism of action has thus far remained obscure. It is generally accepted that Vif-deficient viruses can attach to and penetrate host cells but are blocked at a post-penetration step early in the infection cycle. Yet, comparison of virion morphology or protein composition between wild type and Vif-defective virions has thus far been inconclusive and produced conflicting results. Several reports have suggested that Vif affects the stability of the viral nucleoprotein complex. In particular, NC and reverse transcriptase were found to be less stably associated with viral cores in the absence of Vif. Nevertheless, Vif is generally believed to function within the virus-producing cell. This assumption was largely based on the observation that relatively small amounts of Vif were found to be packaged, with estimates ranging from less than 1 to 100 molecules of Vif per virion. Furthermore, packaging of Vif into virus particles was generally believed to be nonspecific, leading to questions as to the functional significance of Vif incorporation into virions.
Based on this information, we performed an in-depth biochemical analysis of Vif in purified virions from permissive or restrictive host cells to investigate the specificity of Vif incorporation into virions (Khan, 2001). Pulse/chase analysis of single-cycle infected H9 cells did not reveal any Vif-dependent differences in viral protein processing and maturation consistent with recent reports by other investigators. Instead, detergent extraction of purified virions demonstrated an association of Vif with the nucleoprotein complex (Khan, 2001). Quantitative analyses suggest that approximately 10 to 15 percent of total Vif protein is packaged into virions (Khan, 2001). This efficiency is comparable to the 5 percent packaging efficiency reported for the HIV-1 Env protein (Willey, 1988). Interestingly, HIV-1 variants carrying mutations in the nucleocapsid zinc finger domains abolished Vif packaging. In addition, an RNA-packaging defective virus was significantly impaired in packaging of Vif. Finally, deletion of a putative RNA-binding motif between residues 75-114 in Vif abolished its packaging into virions. Virion-associated Vif was resistant to detergent extraction and co-purified with components of the viral nucleoprotein complex and functional reverse transcription complexes (Khan, 2001). Thus, Vif is specifically packaged into virions as a component of the viral nucleoprotein complex. Our data suggest that the specific association of Vif with the viral nucleoprotein complex might be functionally significant and could be a critical requirement for infectivity of viruses produced from restrictive host cells.
Intravirion processing of VifIn investigating the specificity of Vif packaging into virions derived from various cell lines, we noticed that Vif is subjected to intra-virion processing by the HIV-1 protease (Pr) (Khan, 2002). Pr-dependent processing of Vif was observed both in vivo and in vitro. In vivo processing of Vif was cell type-independent and evident by the appearance of a 7-kDa processing product, which was restricted to cell-free virus preparations. Processing of Vif required an active viral protease and was sensitive to protease inhibitors such as ritonavir. The processing site in Vif was characterized both in vivo and in vitro and mapped to Ala150. Interestingly, the Vif processing site is located in a domain that is highly conserved among HIV-1, HIV-2, and simian immunodeficiency virus Vif isolates. Mutations at or near the processing site did not affect protein stability or packaging efficiency but had dramatic effects on Vif processing. In general, mutations that markedly increased or decreased the sensitivity of Vif to proteolytic processing severely impaired or completely abolished Vif function. In contrast, mutations at the same site that had little or no effect on processing efficiency also had no effect on Vif function. None of the mutants affected the ability of the virus to replicate in permissive cell lines. Our data suggest that mutations in Vif that cause a profound change in the sensitivity to Pr-dependent processing also severely impaired Vif function suggesting that intravirion processing of Vif is important for the production of infectious viruses.
HIV-1 Vif is efficiently packaged into virions during productive but not chronic infectionPackaging of the HIV type 1 Vif protein into virus particles is mediated through an interaction with viral genomic RNA and results in the association of Vif with the nucleoprotein complex. Despite the specificity of this process, calculations of the amount of Vif packaged have produced vastly different results. To investigate this apparent discrepancy, we compared the packaging efficiency of Vif into virions derived from acutely and chronically infected H9 cells. We found that Vif was efficiently packaged into virions from acutely infected cells (60 to 100 copies per virion) while packaging into virions from chronically infected H9 cells was near the limit of detection (4 to 6 copies of Vif per virion) (Kao, 2003). Superinfection by an exogenous Vif-defective virus did not rescue packaging of endogenous Vif expressed in the chronically infected culture. In contrast, exogenous Vif expressed by superinfection of wild type virus was readily packaged (30to 40 copies per virion). Biochemical analyses suggest that the differences in the relative packaging efficiencies were not due to gross differences in the steady-state distribution of Vif in chronically or acutely infected cells but are likely due to differences in the relative rates of de novo synthesis of Vif. Despite its low packaging efficiency, endogenously expressed Vif was sufficient to direct the production of viruses with almost wild type infectivity (Kao, 2003). These results provide novel insights into the biochemical properties of Vif and offer an explanation for the reported differences regarding Vif packaging.
Ritu Goila, Ph.D., Visiting Fellow, 301-496-3132, firstname.lastname@example.com; Sandra Kao, M.S., Biologist, 301-496-3132, email@example.com; Mohammod Khan, Ph.D., Research Fellow, 301-496-3132, email@example.com; Eri Miyagi, Ph.D., Visiting Fellow, 301-496-3132, firstname.lastname@example.com; Sandrine Opi, Ph.D., Visiting Fellow, 301-496-3132, firstname.lastname@example.com; Hiroaki Takeuchi, Ph.D., Visiting Fellow, 301-496-3132, email@example.com.
(View list in PubMed.)
Strebel K. HIV-1 Vpu; Putting a Channel to the TASK. Mol Cell. 2004. 14: 150.
Xu H, Svarovskaia ES, Barr R, Zhang Y, Khan MA, Strebel K, Pathak VK. A single amino acid substitution in human APOBEC3G antiretroviral enzyme confers resistance to HIV-1 virion infectivity factor-induced depletion. Proc Natl Acad Sci USA. 2004. 101: 5652.
Nguyen KL, llano M, Akari H, Miyagi E, Poeschla EM, Strebel K, Bour S. Codon optimization of the HIV-1 vpu and vif genes stabilizes their mRNA and allows for highly efficient Rev-independent expression. Virology. 2004. 319: 163.
Akari H, Fujita M, Kao S, Khan MA, Shehu-Xhilaga M, Adachi A, Strebel K. High level expression of human immunodeficiency virus type-1 Vif inhibits viral infectivity by modulating proteolytic processing of the Gag precursor at the p2/nucleocapsid processing site. J Biol Chem. 2004. 279: 12355.
Markovic I, Stantchev TS, Fields KH, Tiffany LJ, Tomic M, Weiss CD, Broder CC, Strebel K, Clouse KA. Thiol/disulfide exchange is a prerequisite for CXCR4-tropic HIV-1 envelope-mediated T-cell fusion during viral entry. Blood. 2004. 103: 1586.
Strebel K. Virus-host interactions: role of HIV proteins Vif, Tat, and Rev. AIDS. 2003. 17 Suppl 4: S25-34.
Varthakavi V, Smith RM, Bour SP, Strebel K, Spearman P. Viral protein U counteracts a human host cell restriction that inhibits HIV-1 particle production. Proc Natl Acad Sci USA. 2003. 100: 15154.
Kao S, Khan MA, Miyagi E, Plishka R, Buckler-White A, Strebel K. The human immunodeficiency virus type 1 Vif protein reduces intracellular expression and inhibits packaging of APOBEC3G (CEM15), a cellular inhibitor of virus infectivity. J Virol. 2003. 77: 11398.
Bour S, Strebel K. The HIV-1 Vpu protein: a multifunctional enhancer of viral particle release. Microbes Infect. 2003. 5: 1029.
Bour S, Akari H, Miyagi E, Strebel K. Naturally occurring amino acid substitutions in the HIV-2 ROD envelope glycoprotein regulate its ability to augment viral particle release. Virology. 2003. 309: 85.
Kao S, Akari H, Khan MA, Dettenhofer M, Yu XF, Strebel K. Human immunodeficiency virus type 1 Vif is efficiently packaged into virions during productive but not chronic infection. J Virol. 2003. 77: 1131.
Khan MA, Akari H, Kao S, Aberham C, Davis D, Buckler-White A, Strebel K. Intravirion processing of the human immunodeficiency virus type 1 Vif protein by the viral protease may be correlated with Vif function. J Virol. 2002. 76: 9112.
Ma C, Marassi FM, Jones DH, Straus SK, Bour S, Strebel K, Schubert U, Oblatt-Montal M, Montal M, Opella SJ. Expression, purification, and activities of full-length and truncated versions of the integral membrane protein Vpu from HIV-1. Protein Sci. 2002. 11: 546.
Akari H, Bour S, Kao S, Adachi A, Strebel K. The human immunodeficiency virus type 1 accessory protein Vpu induces apoptosis by suppressing the nuclear factor kappaB-dependent expression of antiapoptotic factors. J Exp Med. 2001. 194: 1299.
Khan MA, Aberham C, Kao S, Akari H, Gorelick R, Bour S, Strebel K. Human immunodeficiency virus type 1 Vif protein is packaged into the nucleoprotein complex through an interaction with viral genomic RNA. J Virol. 2001. 75: 7252.
Bour S, Perrin C, Akari H, Strebel K. The human immunodeficiency virus type 1 Vpu protein inhibits NF-kappa B activation by interfering with beta TrCP-mediated degradation of Ikappa B. J Biol Chem. 2001. 276: 15920.
Akari H, Arold S, Fukumori T, Okazaki T, Strebel K, Adachi A. Nef-induced major histocompatibility complex class I down-regulation is functionally dissociated from its virion incorporation, enhancement of viral infectivity, and CD4 down-regulation. J Virol. 2000. 74: 2907.
Bour S, Strebel K. HIV accessory proteins: multifunctional components of a complex system. Adv Pharmacol. 2000. 48: 75.
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Talk about wildly appealing! 5 flavors, processed in the U.S.A. under USDA guidelines. You get 5 Sausages, 4 ozs. each, in venison, elk, bison, antelope and hot pepper beef. All perfectly spiced and textured, slow-smoked over hickory and hardwood. They're all naturally lean and low in cholesterol, farm-raised for tender flavor. Note: sorry, no returns unless truly defective.
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Japan's Nikkei Average swings to gain, up 0.2%
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Since the other sign up thread is reaching 5,000 then this is the relaunch of the old thread. Any bios you have in the original sign up thread feel free to post here and if you have any character proposals feel free to post them here also. Have fun
Since the other sign up thread is reaching 5,000 then this is the relaunch of the old thread. Any bios you have in the original sign up thread feel free to post here and if you have any character proposals feel free to post them here also. Have fun
"It isn't jumping the shark if you never come back down." Chuck
First post!
Won 6 Awesome Awards, 2Cool awards, 2 internets, a Raging storm and funniest video award
My RPG Site!
CAU Quantum
TOWAF ( Total Omega Wrestling Alliance Federation)
found it in 1950
previous owner: Micky Borgz
current owner: Manny Chanzi Magaioui ( Tako Supreme)
main arena location- Exdous City
divisions ( structure like Japanese Pro Wrestling)
male championship titles
1 Lightweight championship ( 150lbs to 169lbs
2 Middleweight championship ( 170lbs to 199lbs)
3 Junior heavyweight championship ( 200lbs to 229lbs)
4 Heavyweight championship ( 229lbs to 564lbs)
5 TOWAF World championship
6 TOWAF Tag Team Championship
7 TOWAF Hardcore Championship
Women titles
1 women's Lightweight championship ( 120 to 140lbs)
2 women's Middleweight championship ( 150 to 179lbs
3 women's Junior heavyweight championship ( 180lbs)
4 Women's Heavyweight championship ( 190lbs to 325lbs)
5 women's TOWAF World Championship ( Current Champion- Victoria Stonewall Aka Brickhouse)
6 women's TOWAF Tag Team Championship
7 women's TOWAF Hardcore Championship
both gender title
TOWAF Universal Championship
Roster list 32 males & 32 females for a total roster of 64
Partnerships: CBS for boardcasting rights, and AKI Corporation /Sophia Inc for videogame rights
TOWAF Theme
Black Ice
Victoira Stonewall / Brickhouse's wrestling theme song
Hell Yeah
women Heavyweight main Contenders
1 Victoria Stonewall, AKA Brickhouse
2 Fonna Jargon aka Powerhouse ( height 7'5" weight 315lbs)
theme song
the way of the Warrior
3 Konna Jargon aka Might ( height 7'5" weight 285lbs)
theme song
Black Wind, Fire & Steel
4 Donna Jargon aka Fort ( height 7'5" weight 270lbs)
theme song
Hunting High and Low
5 Ronna Jargon aka Tank ( Height 7'5" weight 260lbs)
theme song
6 Zonna Jargon aka Tower ( height 7'5" weight 250lbs)
theme song
The Kinslayer
7 Yonna Jargon ( height 7'5" 240lbs) aka Freight Train
theme song
Hearts On Fire
8 Cazerig Jargon aka Anvil ( height 6'10" 230lbs)
Fighting the world
Tag Teams
1 The Mighty Amazon sextuplets ( tag member Powerhouse, tag member Might , reserve member Fort, reserve member Tank , reserve member Hammer, and Reserve member Freight Train)
theme song
Stronger Than All
2 Speed & Power (??? & Brickhouse)
1 Melga Mäktig ( The Amazons, and Anvil)
2 Willima Stonewall aka Miss Hammer, & Barracus Aberham Stonewal aka Mr.Stonewall ( Victoria Stonewall / Brickhouse )
please add
Last edited by Bruceleehulk; 04-25-2012 at 08:12 PM.
I say Trukish Wreslting Rules- Hakan
Ps Froggy needs to updated the above link with Usra's powers
I say Trukish Wreslting Rules- Hakan
agent nemo
adrian halworth
they label me a villain cause of how I express my feelings
quick update Bios
CAU Quantum
Name: Abraham XI Hellsbeard aka Agent Abraham
age 60
Height: 7'8"
weight: 565lbs
Build: muscular
Hair: white
eyes: dark blue
Race: Roman / Hybrid Type 3
main ability: high level Acoustokinesis
secondary abilites: class 100 strength, super speed , and super agility
occupation: MI6 Agent
Bio: Captain Abraham XI is the descented of Captain Abraham I, who was the first mate of Captain Orion Legia , before brancing off as his own Captain after her death in 1645 A.D. During his life Captain Aberham was know as the strongest man in the world, and his strength was Legendary. it was said he was capable of holding back over 500 men and many more amazing feats of strength. he was the found of the Dead eye Pirates, and his Descented Captain Abraham XI is the Captain of the 11th Generation of the Dead eye Priates.
the 1st gen Dead Eye Priates, were nobel Pirates, who believed in help the weak and doing what was right, no matter if it might breaking the law. and their successors have kept this tradition alive. during 1685 A.D Captain Abarham had supposedly killed by his own crew in his sleep. and days later after his death it was said that he had rising from the dead, and was giving the title the Immortal pirate by the WBHA, and various other pirates crews during that time.
however Captain Abarham wasn't killed by his own men, he dead peacefully in his sleep, and the person who took up his mantle was his Son Abarham II. trust a tradition was start were when the Previous Captain Abarham , a new one would take his place, give rise to the Immortal Pirate . Captain Abarham XI is the Current Immortal pirate and is the Son of the Previous Immortal Pirate Captain Abarham X. like his father and ancenstors, he is nobel with a strong sense of justice.
and like his ancenstor Captain Abarham I , he is said to be the strongest man in the world. however some people believe that is just a rumor. Captain Abarham is a extremely strong Hybrid with the ability to manipulate sound at a high level. he can manipulateand make sound waves strong enough to one shot entire mountains. however unlike his ancestor Abraham XI didn't become a pirate as the age of priates was long gone, rather he become a agent for MI6.
Captain Abarham and the rest of his follow agents diguises them selfs as pirates / criminals to get investgated the Evil Organization WBHA. his wife Mary was killed by Lester Mcdogual a former MI6 agent who now works for the WBHA.
Name: Abraham XII " Abe" Hellsbeard aka Agent Abe
age: 36
height: 6'0"
weight: 195lbs
hair: black
eyes: light green
Powers: none
weapon: a mystical sword
occupation: MI6 Agent
Bio: Abe is the son of Abarham XI, Abe is the son of Captain Abarham XI, however unlike his father Abe poessesed no powers. he is a mechical genius who has condention his body to peak physical training , through sheer training. he is able to do stuff like flash step because of his training. he is a master swordsman who is capable of handel himself even against super power inviduals.
the sword he carries around with him is a mystical sword that was given to him by Goro. he also uses his mechincal genius to aid him in combat, by making various gadgets, gadgets capable of stand up to super power inviduals. he is Captain Rubber's Idol and had once save a eight year old Captain Rubber from fallen into a deep rocky pit with spikes.
Name: Sebastian Curtis / Agent Curtis
age: 60
Height: 5'6"
weight 165lbs
Hair: dark blue
eyes: light green
Race: Thai / Hybrid type 3
nationality: Thai
main ability: high level Melanokinesis
secondary abillties: danger sense and super agility
occupation: MI6 Agent
Bio: Sebastian Curtis is a MI6 agent who works along side Agent Abraham and his son. he is also Type 3 Hybrid who can manipulated and control Ink allowing him to alter messages , images ,tattoos or anything that is made with ink. he can also generate his own ink and use ink as a means to attack & defend. he's a bite of a joker who isn't overall serious.
Name: Goro D. Wright
age: 54
Height: 6'8"
weight: 325lbs
Hair: black
eyes: dark red
Race: Alien
nationality: British
occupation: MI6 Agent
powers: class 100 strength, a rock hard like hide and has the ability to spout additional arms, can spout up to 100 arms .
sex: male
Bio: Goro D.Wright belongs to a race of alien like golems, who have hard rock skin and the ability to spout additional arms. he is the strong and slient type and rarely speaks. but when he does he talks in a British accent having been born and rise in small town in England. he became a MI6 agent after he befriend Abe, by saving him from rock slide when Abe was just 6 years old.
Name: Alitla Mazanrok AKA Agent Miss Syrup
Age 36
Height: 6'0"
weight: 185lbs
Hair: light green
eyes: dark yellow
race: Alien
Sex: female
nationality: Denmark
home planet: Sucrosalia
Powers: Candy Mimicry (the ability to mimic the traits of any candy substence or Syrup), super agility, 360-Degree Vision ( two eyes in front, one eye on the right side, one eye on the left side and two eyes in the back).
1 can't be hit or sliced while in sticky candy syrup form
2 can make self sticky or intensely solid.
3 shape shifting
4 transform body parts into weapons
5. Harden body to increase toughness
6 can turn into sticky cady syrup to entrap an enemy into her body.
7 has Adhesive secretion
8 can mimic elasticty by turn into sticky candy syrup.
occupation: MI6 Agent
Bio: Alita aka Miss syrup belongs to a race of Aliens that come from a planet that is completey compose of nothing but sweets. everything and everyone on her home planet is basically candy. her speices has four forms, a non candy form, sticky candy syrup form , soft cady form, and hard candy form. they also have the ability to see in multiple driections at once.
she is a MI6 Agent, and she help Abe against a banded of dirty bandits, when she and Abe were 16 years old , 4 years before the became MI6 agents. she has a close releationship with Abe, and is consider to be his girlfriend. she is aslo carrying her's and Abe's child. she likes to greet people with her homeplanet's custom greeting which is rubbing her head against a person , serected sticky candy syrup from her forehead and rubbing it on the person's forehead. when she's bored she often likes to shape shifting into other people.
I say Trukish Wreslting Rules- Hakan
SO okay
Doc's students
The Dude
Cindy and Hacksaw Jr
25 students
BLH this is WAY more than I expected so I'm splitting them into two teams (technically three for Legato's idea) and we'll keep them that way okay?
Team one (the prime squad upperclassmen): trained by Specs, Lang and missions coordinated by Marnie
Team two (younger members less experienced)
Team three (the sub group side team for the first)
The Dude
i'll update Ursa's powers soon but why is it she always gets smacked away or have no effect on the bosses we fight?
Last edited by Froggy; 04-25-2012 at 06:06 PM.
they label me a villain cause of how I express my feelings
Won 6 Awesome Awards, 2Cool awards, 2 internets, a Raging storm and funniest video award
My RPG Site!
Also, just because I can.....
Doughboy Tropes!
-of Blob. Even has similar powers.
-When you can shrug off hits from Eve, even when she's holding back, you've got this.
-Thus far, he hasn't done anything evil and seems to be a pretty cool guy.
-Despite being aware of the power of the Harbinger, he did want to go back and help Fulcrum and Eve.
-While not a genius by any stretch, he is smarter then his appearance would have you think.
-He's got lots of strength and he's tough but he has no real speed.
Won 6 Awesome Awards, 2Cool awards, 2 internets, a Raging storm and funniest video award
My RPG Site!
When in Rome...
Sugar Rush
She's the youngest of Team Insidious, around 19 years of age.
Her best feat is running across the ocean and came close to running around the world before Eve stopped her
When offered to be apart of Team Insidious she accepted it without hesitation
Averted. She's French and she's proud of it but it took alot of bravery on her part to return to where The Protectors and The Justice Legion fought The Harbinger just so she can help Eve and Fulcrum
"It isn't jumping the shark if you never come back down." Chuck
Would it be alright if I tried again? I've rebooted Dragonknight so he has no outside quest or need to go home, which complicated stuff last time.
A lot of people get sentience confused for sapience. Your hamster is sentient, you are sapient. Intelligence is sapience.
Won 6 Awesome Awards, 2Cool awards, 2 internets, a Raging storm and funniest video award
My RPG Site!
A lot of people get sentience confused for sapience. Your hamster is sentient, you are sapient. Intelligence is sapience.
so Agent Nemo's opinion on Captain Justice is while he's one of THE good guys and he likes the fact the guy is on the side of the angels
he always finds it weird how upbeat he is, like the man reminds him that he's not human with how wide his smile is
a bit odd but he's okay with that
and I'm sure Agent Song finds Nemo a bit annoying for hsi lackdaisacal behavior
they label me a villain cause of how I express my feelings