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How long after I put a bid on a foreclosure should we hear back whether or not our offer was approved?
Question by GBsandiego: How long after I put a bid on a foreclosure should we hear back whether or not our offer was approved?
My husband I and I put a bid in on a foreclosure and a short sale yesterday. I know short sales can take weeks and even months to hear back. But, how long on a foreclosure?
Best answer:
Answer by sassy2
12 weeks for a foreclosure.
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3 Responses to "How long after I put a bid on a foreclosure should we hear back whether or not our offer was approved?"
It too can be months before you know anything.
Also weeks or even months but on the whole they tend to have quicker response times than short sales.
Foreclosure can vary between states. Take a look at FL and TX. These states have rather interesting rules in regards to homestead acts in place within the state. In either case, it can take a few months for everythign to fall into place. Also, there are certain things homeowners can do to help delay the process such as paying a small amount to keep their home and restart the foreclosure process all over again. Foreclosures can be tricky, but if all goes well and normal, you can end up with a pretty great deal as the bank just wants to get rid of the debt associated with the property that has not been paid for promptly. Always do your research when dealing with these types of situations. Try to deal with the banks directly or a reputable real estate agent so that the process can be minimal in terms of costliness due to scams and overcharges in fees and so on.


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|Congenic 129S6/SvEvTac mice carrying the spontaneous mutation, Ins2Akita may be useful to combine with other mutations on the 129S6 background for further model development to accelerate or exaggerate diabetic nephropathy and to identify genetic modifiers influencing albuminuria and renal injury in diabetes.
Type Congenic; Spontaneous Mutation; Additional information on Genetically Engineered and Mutant Mice. Visit our online Nomenclature tutorial. Additional information on Congenic nomenclature. Species laboratory mouse Background Strain 129S6-Tac Donor Strain C57BL/6J Donating Investigator Dr. Thomas M Coffman, Duke University Medical Center (AMDCC)
white-bellied black agouti
Congenic 129S6/SvEvTac mice heterozygous for the Ins2 Akita (Akita) spontaneous mutation are viable and fertile. Mice carrying the Akita mutation exhibit hyperglycemia, polydipsia, polyuria and elevated systolic blood pressure when compared to wild-type controls. The diabetic phenotype is more severe and progressive in the male than in the female. Heterozygous males exhibit significantly increased albuminuria and albumin-to-creatine ratios compared to wild-type controls. The absolute level of 129S6-Akita albumin excretion is intermediate when compared to C57BL/6-Ins2Akita/J (Stock No. 003548) being the lowest and D2.B6-Ins2Akita/MatbJ (Stock No. 007562) being the highest. At six months of age, glomerular filtration rates (GFR) are significantly higher in the 129S6-Ins2Akita mice than either wild-type controls or C57BL/6-Ins2Akita/J mice. The kidneys of 6-month old diabetic mice were significantly larger and glomerular volume was also significantly increased when compared to age matched controls. Histopathology of the kidney indicates expanded mesangial matrix of the glomerulus, while the tubular and interstitial regions remain normal (Gurley et. al., 2010).
Islets from Akita heterozygous mice are depleted of beta cells, and the remaining beta cells release very little mature insulin. This, and the finding that mutant mice respond to exogenously administered insulin, indicates that Akita mice can serve as an excellent substitute for mice made insulin dependent diabetic by treatment with alloxan or streptozotocin.
Homozygotes untreated with insulin rarely survive beyond 12 weeks of age.
This strain may be useful to combine with other mutations on the 129S6 background for further model development to accelerate or exaggerate diabetic nephropathy and to identify genetic modifiers influencing albuminuria and renal injury in diabetes.
Ins2Akita is a dominant, spontaneous, point mutation, that introduces a Cys to Tyr substitution at the seventh amino acid in the A chain of mature insulin (amino acid 96 in the preproinsulin II sequence), and results in a major conformational change in the insulin 2 molecule. The Ins2Akita spontaneous mutation on the C57BL/6 background (Stock No. 003548) was backcrossed to 129S6/SvEvTac for 9 generations. All tested SNP markers outside of the congenic region were 129S6 in origin. In 2010, the T1DR received this strain, commonly referred to as 129-Akita, at generation N9 and continues to be maintained on the 129S6-Tac background.
|Wild-type from the colony
|Considerations for Choosing Controls
Strains carrying Ins2Akita allele
013040 B6.Cg-Apoetm1Unc Ins2Akita/J 012628 B6.Cg-Apoetm3(APOE*4)Mae Ins2Akita Ldlrtm1(LDLR)Mae/J 006860 B6.Cg-Ins2Akita Bdkrb2tm1Jfh/SmiJ 006580 B6.Cg-Ins2Akita Ldlrtm1Her/J 004369 B6.Cg-Rag1tm1Mom Ins2Akita/J 003548 C57BL/6-Ins2Akita/J 007562 D2.B6-Ins2Akita/MatbJ 013719 D2.Cg-Apoetm1Unc Ins2Akita/J 006867 FVB.B6-Ins2Akita/MlnJ 008659 NOD.Cg-Rag1tm1Mom Ins2Akita Prf1tm1Sdz/SzJ 014568 NOD.Cg-Rag1tm1Mom Ins2Akita Il2rgtm1Wjl/SzJView Strains carrying Ins2Akita (11 strains)Strains carrying other alleles of Ins2
012943 C57BL/6-Tg(Ins2-luc/EGFP/TK)300Kauf/J 005739 NOD-Tg(H2-Ea-Ins2)1Wehi/WehiJ 005353 NOD.129-(D7Mit105-D7Mit223)/GseJ 005036 NOD.129S2(B6)-Ins2tm1Jja/GseJ 013116 NOD.B6-Tg(Ins2-luc/EGFP/TK)300Kauf/J 005524 NOD.Cg-Tg(Ins2*Y16A)1Ell Ins1tm1Jja Ins2tm1Jja/GseJ 005525 NOD.Cg-Tg(Ins2*Y16A)3Ell Ins1tm1Jja Ins2tm1Jja/GseJView Strains carrying other alleles of Ins2 (7 strains)
View Related Disease (OMIM) TermsRelated Disease (OMIM) Terms provided by MGI
- Model with phenotypic similarity to human disease where etiologies involve orthologs. Human genes are associated with this disease. Orthologs of those genes appear in the mouse genotype(s).Diabetes Mellitus, Permanent Neonatal; PNDM- Model with phenotypic similarity to human disease where etiologies are distinct. Human genes are associated with this disease. Orthologs of these genes do not appear in the mouse genotype(s).
Diabetes Mellitus, Insulin-Dependent; IDDMModels with phenotypic similarity to human diseases where etiology is unknown or involving genes where ortholog is unknown.
Diabetes Mellitus, Noninsulin-Dependent; NIDDM
Maturity-Onset Diabetes of the Young; MODY
- Potential model based on gene homology relationships. Phenotypic similarity to the human disease has not been tested.Diabetes Mellitus, Insulin-Dependent, 2 (INS)
Hyperproinsulinemia (INS)
Maturity-Onset Diabetes of the Young, Type 10; MODY10 (INS)
View Mammalian Phenotype TermsMammalian Phenotype Terms provided by MGIassigned by genotype
The following phenotype information is associated with a similar, but not exact match to this JAX® Mice strain.
- mortality/aging
- premature death
- homeostasis/metabolism phenotype
- decreased circulating insulin level
- insulin levels are decreased in the blood and pancreas (MGI Ref ID J:40063)
- decreased insulin secretion
- hyperglycemia
- impaired glucose tolerance (MGI Ref ID J:40063)
- endocrine/exocrine gland phenotype
- abnormal Leydig cell morphology
- mutant males display some pigmented vacuoles in Leydig cells in the testes, but to a lesser extent than in double mutant males at 12 months of age (MGI Ref ID J:108948)
- abnormal pancreatic beta cell morphology
- degranulated pancreatic beta cells
- partial degranulation (MGI Ref ID J:47883)
- decreased insulin secretion
- renal/urinary system phenotype
- hydronephrosis
- seen in all diabetic males but only 5 of 20 diabetic females (MGI Ref ID J:40063)
- polyuria
- develops soon after weaning and is more severe in males (MGI Ref ID J:40063)
- behavior/neurological phenotype
- akinesia
- 7-8 week old males exhibit increased immobility time as measured in open field test (MGI Ref ID J:125256)
- hypoactivity
- increased anxiety-related response
- increased fluid intake
- 7-8 week old males consume 7 fold more water as compared to controls (33.28 ml/day v. 4.68 ml/day) (MGI Ref ID J:125256)
- polydipsia
- develops soon after weaning and is more severe in males (MGI Ref ID J:40063)
- polyphagia
- 7-8 week old males consume 2 fold more food as compared to controls (8.16 g/day v. 4.48 g/day) (MGI Ref ID J:125256)
- growth/size/body region phenotype
- decreased body weight
- 7-8 week old males exhibit decreased weight as compared to controls (24g v. 26g) (MGI Ref ID J:125256)
- postnatal growth retardation
- weight gain is normal through 18 weeks of age but then no further weight gain is seen and by 30 weeks weight loss is observed (MGI Ref ID J:40063)
- adipose tissue phenotype
- decreased subcutaneous adipose tissue amount
- mutants have almost no subcutaneous fat (MGI Ref ID J:108948)
- cellular phenotype
- abnormal mitochondrion morphology
- mutant mice show greater mitochondrial damage than wild-type or Bdkrb2-deficient mice at 12 months of age (MGI Ref ID J:108948)
- reproductive system phenotype
- abnormal Leydig cell morphology
- mutant males display some pigmented vacuoles in Leydig cells in the testes, but to a lesser extent than in double mutant males at 12 months of age (MGI Ref ID J:108948)
- skeleton phenotype
- decreased bone mineral density
- mutants have significantly reduced bone density compared to wild-type or Bdkrb2-deficient mice (MGI Ref ID J:108948)
- kyphosis
- diabetic mice display kyphosis but to a lesser extent than double mutant mice (MGI Ref ID J:108948)
- integument phenotype
- decreased subcutaneous adipose tissue amount
- mutants have almost no subcutaneous fat (MGI Ref ID J:108948)
Ins2Akita/Ins2+involves: C3H * C57BL/6NJcl * C57BL/6NSlc
- homeostasis/metabolism phenotype
- hyperglycemia
- progressive increase in morning blood glucose level is seen (MGI Ref ID J:40063)
- impaired glucose tolerance (MGI Ref ID J:40063)
- homeostasis/metabolism phenotype
- hyperglycemia (MGI Ref ID J:99412)
- heterozygous males and females are hyperglycemic by 6 weeks of age (plasma glucose - 325 mg/dL); at 12 and 18 weeks of age, plasma glucose levels in males have appproximately doubled (645 mg/dL and 666 mg/dL) while levels in female mutants have increased much less (341 and 298 mg/dL respectively) (MGI Ref ID J:76224)
- increased insulin sensitivity
- diabetic males that are hyperglycemic (plasma glucose - ~660 mg/dL) at 12 weeks show a return to euglycemia one hour after receiving 1 unit of insulin, demonstrating insulin sensitivity (MGI Ref ID J:76224)
- immune system phenotype
- abnormal microglial cell morphology
- after 31-36 weeks of hyperglycemia, retinal microglia have a reactive morphology (MGI Ref ID J:99412)
- abnormal response to transplant
- hyperglycemic male mice transplanted with pancreatic islets from wild-type B6 males become euglycemic in one week after transplant and remain euglycemic until removal of the graft (8 weeks); male mice receiving an allogeneic transplant of BALB/c wild-type islets initially become euglycemic but revert to hyperglycemia because of rejection of the graft (MGI Ref ID J:76224)
- increased leukocyte cell number
- after 31-36 weeks of hyperglycemia, the number of leukocytes per retina is increased (MGI Ref ID J:99412)
- cardiovascular system phenotype
- abnormal retinal vasculature morphology
- after 31-36 weeks of hyperglycemia, a modest increase in the number of acellular capillaries is seen in the retina (MGI Ref ID J:99412)
- increased vascular permeability
- vascular permeability is increased in the retina (MGI Ref ID J:99412)
- growth/size/body region phenotype
- decreased body weight
- at death heterozygous males weigh significantly less than wild-type males (MGI Ref ID J:99412)
- nervous system phenotype
- abnormal astrocyte morphology
- after 31-36 weeks of hyperglycemia, astrocytes close to large caliber superficial blood vessels in the retina have short projections that do not conjoin with the vessel (MGI Ref ID J:99412)
- abnormal microglial cell morphology
- after 31-36 weeks of hyperglycemia, retinal microglia have a reactive morphology (MGI Ref ID J:99412)
- vision/eye phenotype
- abnormal retinal apoptosis
- after 31-36 weeks of hyperglycemia, significantly more caspase-3 positive cells are seen (MGI Ref ID J:99412)
- abnormal retinal neuronal layer morphology
- after 22 weeks of hyperglycemia, in the peripheral regions the inner nuclear layer and inner plexiform layer thickness are reduced by 15.6% and 27%, respectively, and in the central region the thickness of the inner plexiform layer is reduced by 16.7% (MGI Ref ID J:99412)
- abnormal retinal ganglion layer morphology
- after 22 weeks of hyperglycemia, the number of nuclei in the retinal ganglion cell layer is reduced by 23.4% (MGI Ref ID J:99412)
- abnormal retinal vasculature morphology
- after 31-36 weeks of hyperglycemia, a modest increase in the number of acellular capillaries is seen in the retina (MGI Ref ID J:99412)
- hematopoietic system phenotype
- abnormal microglial cell morphology
- after 31-36 weeks of hyperglycemia, retinal microglia have a reactive morphology (MGI Ref ID J:99412)
- increased leukocyte cell number
- after 31-36 weeks of hyperglycemia, the number of leukocytes per retina is increased (MGI Ref ID J:99412)
- cellular phenotype
- abnormal retinal apoptosis
- after 31-36 weeks of hyperglycemia, significantly more caspase-3 positive cells are seen (MGI Ref ID J:99412)
- homeostasis/metabolism phenotype
- albuminuria
- 3-fold increase in albumin-to-creatine ratio at 4 months of age, however albuminuria does not persist at 6 months of age (MGI Ref ID J:198186)
- renal/urinary system phenotype
- albuminuria
- 3-fold increase in albumin-to-creatine ratio at 4 months of age, however albuminuria does not persist at 6 months of age (MGI Ref ID J:198186)
- expanded mesangial matrix
- mesangial matrix expansion is seen at 4 months of age (MGI Ref ID J:198186)
- glomerulosclerosis
- same degree of glomerular injury as in homozygotes at 6 months of age (MGI Ref ID J:198186)
- increased renal glomerular filtration rate
- glomerular filtration rate is increased at 6 months of age (MGI Ref ID J:198186)
Ins2Akita/Ins2+involves: C57BL/6NSlc
- homeostasis/metabolism phenotype
- *normal* homeostasis/metabolism phenotype
- mice exhibit normal insulin sensitivity (MGI Ref ID J:200802)
- endocrine/exocrine gland phenotype
- abnormal pancreatic islet morphology
- beta cells contain a small number of secretory granules, a tubulovesicular structure comprised of enlarged endoplasmic reticulum, and swelling or disruption of mitochondria (MGI Ref ID J:200802)
- decreased insulin secretion
- decreased total pancreatic insulin and prolinsulin content (MGI Ref ID J:200802)
- growth/size/body region phenotype
- decreased body weight (MGI Ref ID J:200802)
- behavior/neurological phenotype
- increased food intake (MGI Ref ID J:200802)
- mortality/aging
- postnatal lethality (MGI Ref ID J:47883)
- homeostasis/metabolism phenotype
- decreased insulin secretion
- the pancreatic ratio of insulin to glucagon is decreased to 0.21 and 0.01 at birth and 14 days of age, respectively, compared to 1.17 and 1.11 in wild-type mice (MGI Ref ID J:47883)
- hyperglycemia
- blood glucose levels are slightly higher at 1 day of age and much higher at 14 days of age with no gender differences seen (MGI Ref ID J:47883)
- endocrine/exocrine gland phenotype
- abnormal pancreatic alpha cell morphology
- alpha cell density is markedly increased (MGI Ref ID J:47883)
- abnormal pancreatic beta cell morphology
- decreased insulin secretion
- the pancreatic ratio of insulin to glucagon is decreased to 0.21 and 0.01 at birth and 14 days of age, respectively, compared to 1.17 and 1.11 in wild-type mice (MGI Ref ID J:47883)
- small pancreatic islets
- islet area is reduced (MGI Ref ID J:47883)
- mortality/aging
- premature death
- untreated homozygous mice rarely survive past 12 weeks of age, with death resulting from extreme hyperglycemia; (MGI Ref ID J:76224)
- homeostasis/metabolism phenotype
- hyperglycemia
- homozygous mice rapidly become hyperglycemic (MGI Ref ID J:76224)
Ins2Akita/Ins2Akitainvolves: C57BL/6NSlc
- endocrine/exocrine gland phenotype
- abnormal pancreas physiology
- expression of a proliferation marker in the pancreas islet is decreased compared to in wild-type mice (MGI Ref ID J:156725)
- decreased pancreatic beta cell mass
- in 50% of mice at 8 weeks (MGI Ref ID J:156725)
- homeostasis/metabolism phenotype
- decreased circulating insulin level (MGI Ref ID J:156725)
- decreased insulin secretion
- pancreas insulin levels are lower than in Cebpbtm1.1Maka homozygotes (MGI Ref ID J:156725)
- hyperglycemia (MGI Ref ID J:156725)
- cardiovascular system phenotype
- hematoma
- greater hematoma expansion induced by autologous blood injection in diabetic mice (MGI Ref ID J:168556)
- cellular phenotype
- abnormal pancreatic islet cell apoptosis
- expression of apoptosis markers in the pancreas islet is increased compared to in wild-type mice (MGI Ref ID J:156725)
- mortality/aging
- premature death
- approximately 20% of mutants fail to thrive and are sacrificed at 6 months of age (MGI Ref ID J:198186)
- cardiovascular system phenotype
- abnormal glomerular capillary morphology
- mice show a decrease in CD31 positive structures in the glomeruli, indicating collapse of the glomerular tufts (MGI Ref ID J:198186)
- growth/size/body region phenotype
- decreased body weight
- reduced body weight at 4 and 6 months of age (MGI Ref ID J:198186)
- homeostasis/metabolism phenotype
- albuminuria
- 3-fold increase in albumin-to-creatine ratio at 4 months of age; albuminuria persists in mutants at 6 months of age (MGI Ref ID J:198186)
- hyperglycemia (MGI Ref ID J:198186)
- renal/urinary system phenotype
- abnormal kidney interstitium morphology
- abnormal renal glomerulus morphology
- increase in glomerular collagen IV deposition at 6 months of age (MGI Ref ID J:198186)
- abnormal glomerular capillary morphology
- mice show a decrease in CD31 positive structures in the glomeruli, indicating collapse of the glomerular tufts (MGI Ref ID J:198186)
- expanded mesangial matrix
- mesangial matrix expansion is seen at 4 months of age and is more pronounced than in heterozygous mice (MGI Ref ID J:198186)
- glomerulosclerosis
- same degree of glomerular injury as in heterozygotes at 6 months of age (MGI Ref ID J:198186)
- albuminuria
- 3-fold increase in albumin-to-creatine ratio at 4 months of age; albuminuria persists in mutants at 6 months of age (MGI Ref ID J:198186)
- increased renal glomerular filtration rate
- glomerular filtration rate is increased at 4 months of age but decreased by 6 months of age to normal levels (MGI Ref ID J:198186)
- increased renal glomerulus basement membrane thickness (MGI Ref ID J:198186)
Ins2Akita/?involves: C57BL/6NSlc
- growth/size/body region phenotype
- decreased body weight (MGI Ref ID J:130021)
- adipose tissue phenotype
- abnormal adipocyte glucose uptake
- abnormal adipose tissue amount
- whole body fat mass is reduced at 8 and 3 weeks of age, however whole body lean mass is no different from wild-type (MGI Ref ID J:130021)
- behavior/neurological phenotype
- hypoactivity
- mutants are less active during a 24 hour cycle (MGI Ref ID J:130021)
- increased food intake
- daily food intake is increased twofold (MGI Ref ID J:130021)
- homeostasis/metabolism phenotype
- abnormal glucose homeostasis
- during hyperinsulinemic-euglycemic clamps, mutants show a 40% reduction in insulin-stimulated whole body glucose turnover (MGI Ref ID J:130021)
- basal hepatic glucose production is increased (MGI Ref ID J:130021)
- hepatic glucose production remains elevated during the insulin clamp unlike in wild-type mice which show a decrease (MGI Ref ID J:130021)
- during hyperinsulinemic-euglycemic clamps, insulin-stimulated whole body glycolysis and glycogen plus lipid synthesis are reduced by 40-50% (MGI Ref ID J:130021)
- decreased circulating insulin level
- fed insulin levels are reduced (MGI Ref ID J:130021)
- hyperglycemia
- mutants develop overnight-fasted hyperglycemia (MGI Ref ID J:130021)
- insulin resistance
- nonobese mutants develop insulin resistance in skeletal muscle, liver, and brown adipose tissue, as indicated by an approximate 80% reduction in glucose infusion rate during hyperinsulinemic-euglycemic clamps (MGI Ref ID J:130021)
- chronic treatment with phloridzin to chronically lower circulating glucose levels normalizes peripheral insulin action but does not normalize hepatic insulin action (MGI Ref ID J:130021)
- decreased respiratory quotient
- respiratory exchange ratio is reduced, indicating increased lipid oxidation (MGI Ref ID J:130021)
- decreased triglyceride level
- during hyperinsulinemic-euglycemic clamps, intramuscular triglyceride levels are reduced by almost 90% (MGI Ref ID J:130021)
- decreased circulating triglyceride level
- following an overnight fast and phloridzin treatment to lower plasma glucose levels, basal plasma triglyceride levels are reduced by 40% (MGI Ref ID J:130021)
- however, the insulin clamp has no effect on plasma triglyceride levels in mutants compared to wild-type mice in which there is a 50% reduction (MGI Ref ID J:130021)
- decreased liver triglyceride level
- intrahepatic triglyceride levels are reduced during hyperinsulinemic-euglycemic clamps (MGI Ref ID J:130021)
- increased carbon dioxide production
- both rate of oxygen consumption and carbon dioxide production are increased by about 40% (MGI Ref ID J:130021)
- increased energy expenditure
- mutants show increased energy expenditure during a 24 hour cycle (MGI Ref ID J:130021)
- increased oxygen consumption
- both rate of oxygen consumption and carbon dioxide production are increased by about 40% (MGI Ref ID J:130021)
- cardiovascular system phenotype
- abnormal cardiac muscle contractility
- abnormal heart morphology
- cardiac remodeling (MGI Ref ID J:130021)
- liver/biliary system phenotype
- decreased liver triglyceride level
- intrahepatic triglyceride levels are reduced during hyperinsulinemic-euglycemic clamps (MGI Ref ID J:130021)
- muscle phenotype
- abnormal cardiac muscle contractility
- abnormal muscle cell glucose uptake
- cellular phenotype
- abnormal muscle cell glucose uptakeView Research ApplicationsResearch ApplicationsThis mouse can be used to support research in many areas including:
Ins2Akita related
Internal/Organ Research
Kidney Defects
Cell Biology Research
Protein Processing
Diabetes and Obesity Research
Impaired Insulin Processing
Insulin Receptors and Growth Factors
Islet Transplantation Studies
Type 1 Diabetes (IDDM)
MODY, mature onset diabetes of the young
Endocrine Deficiency Research
Pancreas Defects
|Allele Symbol
|Allele Name
|Allele Type
|Common Name(s)
|Akita; AkitaIns2; Ins2C96Y; Ins2Mody; Mody; Mody4;
|Strain of Origin
|Gene Symbol and Name
|Ins2, insulin II
|Gene Common Name(s)
|AA986540; IDDM; IDDM1; IDDM2; ILPR; IRDN; Ins-2; InsII; MODY10; Mody; Mody4; expressed sequence AA986540; maturity onset diabetes of the young; maturity onset diabetes of the young 4;
|General Note
|Phenotypic Similarity to Human Syndrome: Type 1 Diabetic Macrovascular Disease (J:174983)
|Molecular Note
|In the mutant allele a transition from G to A at nucleotide 1907 disrupted an Fnu4HI site in exon 3. This mutation changed the seventh amino acid in the A chain of mature insulin, Cys96 (TGC), to Tyr (TAC). The authors predict that the transition would disrupt a disulfide bond between the A and the B chains and would likely induce a major conformational change in insulin 2 molecules. RT-PCR studies suggest that both normal and mutant Ins2 alleles are transcribed similarly in pancreatic islets of heterozygous mice, although immunofluorescence and immunoblot analyses of heterozygous islets detected reduced levels of insulin and proinsulin. [MGI Ref ID J:51935]
Genotyping ProtocolsIns2Akita, End Point Analysis
Helpful LinksGenotyping resources and troubleshooting
Gurley SB; Mach CL; Stegbauer J; Yang J; Snow KP; Hu A; Meyer TW; Coffman TM. 2010. Influence of genetic background on albuminuria and kidney injury in Ins2(+/C96Y) (Akita) mice. Am J Physiol Renal Physiol 298(3):F788-95. [PubMed: 20042456] [MGI Ref ID J:157873]
Ins2Akita related
Abudukadier A; Fujita Y; Obara A; Ohashi A; Fukushima T; Sato Y; Ogura M; Nakamura Y; Fujimoto S; Hosokawa M; Hasegawa H; Inagaki N. 2013. Tetrahydrobiopterin has a glucose-lowering effect by suppressing hepatic gluconeogenesis in an endothelial nitric oxide synthase-dependent manner in diabetic mice. Diabetes 62(9):3033-43. [PubMed: 23649519] [MGI Ref ID J:208962]
Aghdam SY; Gurel Z; Ghaffarieh A; Sorenson CM; Sheibani N. 2013. High glucose and diabetes modulate cellular proteasome function: Implications in the pathogenesis of diabetes complications. Biochem Biophys Res Commun 432(2):339-44. [PubMed: 23391566] [MGI Ref ID J:198848]
Akimov NP; Renteria RC. 2012. Spatial frequency threshold and contrast sensitivity of an optomotor behavior are impaired in the Ins2Akita mouse model of diabetes. Behav Brain Res 226(2):601-5. [PubMed: 21963766] [MGI Ref ID J:180197]
Asakawa A; Toyoshima M; Inoue K; Koizumi A. 2007. Ins2Akita mice exhibit hyperphagia and anxiety behavior via the melanocortin system. Int J Mol Med 19(4):649-52. [PubMed: 17334640] [MGI Ref ID J:125256]
Awad AS; Kinsey GR; Khutsishvili K; Gao T; Bolton WK; Okusa MD. 2011. Monocyte/macrophage chemokine receptor CCR2 mediates diabetic renal injury. Am J Physiol Renal Physiol 301(6):F1358-66. [PubMed: 21880831] [MGI Ref ID J:180042]
Bachar-Wikstrom E; Wikstrom JD; Ariav Y; Tirosh B; Kaiser N; Cerasi E; Leibowitz G. 2013. Stimulation of autophagy improves endoplasmic reticulum stress-induced diabetes. Diabetes 62(4):1227-37. [PubMed: 23274896] [MGI Ref ID J:208584]
Barber AJ; Antonetti DA; Kern TS; Reiter CE; Soans RS; Krady JK; Levison SW; Gardner TW; Bronson SK. 2005. The Ins2Akita mouse as a model of early retinal complications in diabetes. Invest Ophthalmol Vis Sci 46(6):2210-8. [PubMed: 15914643] [MGI Ref ID J:99412]
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Okamoto K; Iwasaki N; Doi K; Noiri E; Iwamoto Y; Uchigata Y; Fujita T; Tokunaga K. 2012. Inhibition of glucose-stimulated insulin secretion by KCNJ15, a newly identified susceptibility gene for type 2 diabetes. Diabetes 61(7):1734-41. [PubMed: 22566534] [MGI Ref ID J:203172]
Oudit GY; Liu GC; Zhong J; Basu R; Chow FL; Zhou J; Loibner H; Janzek E; Schuster M; Penninger JM; Herzenberg AM; Kassiri Z; Scholey JW. 2010. Human recombinant ACE2 reduces the progression of diabetic nephropathy. Diabetes 59(2):529-38. [PubMed: 19934006] [MGI Ref ID J:164158]
Oyadomari S; Koizumi A; Takeda K; Gotoh T; Akira S; Araki E; Mori M. 2002. Targeted disruption of the Chop gene delays endoplasmic reticulum stress-mediated diabetes. J Clin Invest 109(4):525-32. [PubMed: 11854325] [MGI Ref ID J:74700]
Oyadomari S; Yun C; Fisher EA; Kreglinger N; Kreibich G; Oyadomari M; Harding HP; Goodman AG; Harant H; Garrison JL; Taunton J; Katze MG; Ron D. 2006. Cotranslocational degradation protects the stressed endoplasmic reticulum from protein overload. Cell 126(4):727-39. [PubMed: 16923392] [MGI Ref ID J:115988]
Park HJ; Zhang Y; Du C; Welzig CM; Madias C; Aronovitz MJ; Georgescu SP; Naggar I; Wang B; Kim YB; Blaustein RO; Karas RH; Liao R; Mathews CE; Galper JB. 2009. Role of SREBP-1 in the development of parasympathetic dysfunction in the hearts of type 1 diabetic Akita mice. Circ Res 105(3):287-94. [PubMed: 19423844] [MGI Ref ID J:164764]
Patel VB; Bodiga S; Basu R; Das SK; Wang W; Wang Z; Lo J; Grant MB; Zhong J; Kassiri Z; Oudit GY. 2012. Loss of angiotensin-converting enzyme-2 exacerbates diabetic cardiovascular complications and leads to systolic and vascular dysfunction: a critical role of the angiotensin II/AT1 receptor axis. Circ Res 110(10):1322-35. [PubMed: 22474255] [MGI Ref ID J:212515]
Pearson T; Shultz LD; Lief J; Burzenski L; Gott B; Chase T; Foreman O; Rossini AA; Bottino R; Trucco M; Greiner DL. 2008. A new immunodeficient hyperglycaemic mouse model based on the Ins2 ( Akita ) mutation for analyses of human islet and beta stem and progenitor cell function. Diabetologia 51(8):1449-56. [PubMed: 18563383] [MGI Ref ID J:138005]
Pendse AA; Johnson LA; Tsai YS; Maeda N. 2010. Pparg-P465L mutation worsens hyperglycemia in Ins2-Akita female mice via adipose-specific insulin resistance and storage dysfunction. Diabetes 59(11):2890-7. [PubMed: 20724579] [MGI Ref ID J:169338]
Pfister F; Feng Y; vom Hagen F; Hoffmann S; Molema G; Hillebrands JL; Shani M; Deutsch U; Hammes HP. 2008. Pericyte migration: a novel mechanism of pericyte loss in experimental diabetic retinopathy. Diabetes 57(9):2495-502. [PubMed: 18559662] [MGI Ref ID J:141775]
Proctor G; Jiang T; Iwahashi M; Wang Z; Li J; Levi M. 2006. Regulation of renal fatty acid and cholesterol metabolism, inflammation, and fibrosis in Akita and OVE26 mice with type 1 diabetes. Diabetes 55(9):2502-9. [PubMed: 16936198] [MGI Ref ID J:116591]
Pulinilkunnil T; Kienesberger PC; Nagendran J; Waller TJ; Young ME; Kershaw EE; Korbutt G; Haemmerle G; Zechner R; Dyck JR. 2013. Myocardial adipose triglyceride lipase overexpression protects diabetic mice from the development of lipotoxic cardiomyopathy. Diabetes 62(5):1464-77. [PubMed: 23349479] [MGI Ref ID J:208574]
Queisser MA; Yao D; Geisler S; Hammes HP; Lochnit G; Schleicher ED; Brownlee M; Preissner KT. 2010. Hyperglycemia impairs proteasome function by methylglyoxal. Diabetes 59(3):670-8. [PubMed: 20009088] [MGI Ref ID J:164153]
Rajab M; Jin H; Welzig CM; Albano A; Aronovitz M; Zhang Y; Park HJ; Link MS; Noujaim SF; Galper JB. 2013. Increased inducibility of ventricular tachycardia and decreased heart rate variability in a mouse model for type 1 diabetes: effect of pravastatin. Am J Physiol Heart Circ Physiol 305(12):H1807-16. [PubMed: 24163078] [MGI Ref ID J:207722]
Rakoczy EP; Ali Rahman IS; Binz N; Li CR; Vagaja NN; de Pinho M; Lai CM. 2010. Characterization of a mouse model of hyperglycemia and retinal neovascularization. Am J Pathol 177(5):2659-70. [PubMed: 20829433] [MGI Ref ID J:166270]
Ron D. 2002. Proteotoxicity in the endoplasmic reticulum: lessons from the Akita diabetic mouse. J Clin Invest 109(4):443-5. [PubMed: 11854314] [MGI Ref ID J:78863]
Rudchenko A; Akude E; Cooper E. 2014. Synapses on sympathetic neurons and parasympathetic neurons differ in their vulnerability to diabetes. J Neurosci 34(26):8865-74. [PubMed: 24966386] [MGI Ref ID J:212541]
Salem ES; Grobe N; Elased KM. 2014. Insulin treatment attenuates renal ADAM17 and ACE2 shedding in diabetic Akita mice. Am J Physiol Renal Physiol 306(6):F629-39. [PubMed: 24452639] [MGI Ref ID J:207415]
Schmidt RE; Feng D; Wang Q; Green KG; Snipes LL; Yamin M; Brines M. 2011. Effect of insulin and an erythropoietin-derived peptide (ARA290) on established neuritic dystrophy and neuronopathy in Akita (Ins2 Akita) diabetic mouse sympathetic ganglia. Exp Neurol 232(2):126-35. [PubMed: 21872588] [MGI Ref ID J:178385]
Schmidt RE; Green KG; Snipes LL; Feng D. 2009. Neuritic dystrophy and neuronopathy in Akita (Ins2(Akita)) diabetic mouse sympathetic ganglia. Exp Neurol 216(1):207-18. [PubMed: 19111542] [MGI Ref ID J:146204]
Schoeller EL; Albanna G; Frolova AI; Moley KH. 2012. Insulin rescues impaired spermatogenesis via the hypothalamic-pituitary-gonadal axis in Akita diabetic mice and restores male fertility. Diabetes 61(7):1869-78. [PubMed: 22522616] [MGI Ref ID J:203174]
Schoeller EL; Chi M; Drury A; Bertschinger A; Esakky P; Moley KH. 2014. Leptin monotherapy rescues spermatogenesis in male Akita type 1 diabetic mice. Endocrinology 155(8):2781-6. [PubMed: 24840347] [MGI Ref ID J:214314]
Schrufer TL; Antonetti DA; Sonenberg N; Kimball SR; Gardner TW; Jefferson LS. 2010. Ablation of 4E-BP1/2 prevents hyperglycemia-mediated induction of VEGF expression in the rodent retina and in Muller cells in culture. Diabetes 59(9):2107-16. [PubMed: 20547975] [MGI Ref ID J:169349]
Shi Y; Lo CS; Chenier I; Maachi H; Filep JG; Ingelfinger JR; Zhang SL; Chan JS. 2013. Overexpression of catalase prevents hypertension and tubulointerstitial fibrosis and normalization of renal angiotensin-converting enzyme-2 expression in Akita mice. Am J Physiol Renal Physiol 304(11):F1335-46. [PubMed: 23552863] [MGI Ref ID J:197243]
Shirakawa J; Togashi Y; Sakamoto E; Kaji M; Tajima K; Orime K; Inoue H; Kubota N; Kadowaki T; Terauchi Y. 2013. Glucokinase activation ameliorates ER stress-induced apoptosis in pancreatic beta-cells. Diabetes 62(10):3448-58. [PubMed: 23801577] [MGI Ref ID J:208951]
Sklavos MM; Bertera S; Tse HM; Bottino R; He J; Beilke JN; Coulombe MG; Gill RG; Crapo JD; Trucco M; Piganelli JD. 2010. Redox modulation protects islets from transplant-related injury. Diabetes 59(7):1731-8. [PubMed: 20413509] [MGI Ref ID J:169646]
Smith SB; Duplantier J; Dun Y; Mysona B; Roon P; Martin PM; Ganapathy V. 2008. In vivo protection against retinal neurodegeneration by sigma receptor 1 ligand (+)-pentazocine. Invest Ophthalmol Vis Sci 49(9):4154-61. [PubMed: 18469181] [MGI Ref ID J:141696]
Soto I; Howell GR; John CW; Kief JL; Libby RT; John SW. 2014. DBA/2J Mice Are Susceptible to Diabetic Nephropathy and Diabetic Exacerbation of IOP Elevation. PLoS One 9(9):e107291. [PubMed: 25207540] [MGI Ref ID J:213912]
Takeshita S; Moritani M; Kunika K; Inoue H; Itakura M. 2006. Diabetic modifier QTLs identified in F2 intercrosses between Akita and A/J mice. Mamm Genome 17(9):927-40. [PubMed: 16964447] [MGI Ref ID J:112869]
Tchekneva EE; Rinchik EM; Polosukhina D; Davis LS; Kadkina V; Mohamed Y; Dunn SR; Sharma K; Qi Z; Fogo AB; Breyer MD. 2007. A sensitized screen of N-ethyl-N-nitrosourea-mutagenized mice identifies dominant mutants predisposed to diabetic nephropathy. J Am Soc Nephrol 18(1):103-12. [PubMed: 17151334] [MGI Ref ID J:135943]
Toque HA; Nunes KP; Yao L; Xu Z; Kondrikov D; Su Y; Webb RC; Caldwell RB; Caldwell RW. 2013. Akita spontaneously type 1 diabetic mice exhibit elevated vascular arginase and impaired vascular endothelial and nitrergic function. PLoS One 8(8):e72277. [PubMed: 23977269] [MGI Ref ID J:206426]
Umino Y; Solessio E. 2013. Loss of scotopic contrast sensitivity in the optomotor response of diabetic mice. Invest Ophthalmol Vis Sci 54(2):1536-43. [PubMed: 23287790] [MGI Ref ID J:214570]
Vagaja NN; Chinnery HR; Binz N; Kezic JM; Rakoczy EP; McMenamin PG. 2012. Changes in murine hyalocytes are valuable early indicators of ocular disease. Invest Ophthalmol Vis Sci 53(3):1445-51. [PubMed: 22297487] [MGI Ref ID J:196754]
Vallon V; Gerasimova M; Rose MA; Masuda T; Satriano J; Mayoux E; Koepsell H; Thomson SC; Rieg T. 2014. SGLT2 inhibitor empagliflozin reduces renal growth and albuminuria in proportion to hyperglycemia and prevents glomerular hyperfiltration in diabetic Akita mice. Am J Physiol Renal Physiol 306(2):F194-204. [PubMed: 24226524] [MGI Ref ID J:205116]
Vallon V; Rose M; Gerasimova M; Satriano J; Platt KA; Koepsell H; Cunard R; Sharma K; Thomson SC; Rieg T. 2013. Knockout of Na-glucose transporter SGLT2 attenuates hyperglycemia and glomerular hyperfiltration but not kidney growth or injury in diabetes mellitus. Am J Physiol Renal Physiol 304(2):F156-67. [PubMed: 23152292] [MGI Ref ID J:192346]
Vashistha H; Singhal PC; Malhotra A; Husain M; Mathieson P; Saleem MA; Kuriakose C; Seshan S; Wilk A; Delvalle L; Peruzzi F; Giorgio M; Pelicci PG; Smithies O; Kim HS; Kakoki M; Reiss K; Meggs LG. 2012. Null mutations at the p66 and bradykinin 2 receptor loci induce divergent phenotypes in the diabetic kidney. Am J Physiol Renal Physiol 303(12):F1629-40. [PubMed: 23019230] [MGI Ref ID J:190320]
Wang CH; Li F; Hiller S; Kim HS; Maeda N; Smithies O; Takahashi N. 2011. A modest decrease in endothelial NOS in mice comparable to that associated with human NOS3 variants exacerbates diabetic nephropathy. Proc Natl Acad Sci U S A 108(5):2070-5. [PubMed: 21245338] [MGI Ref ID J:169115]
Wang J; Chen Y; Yuan Q; Tang W; Zhang X; Osei K. 2011. Control of Precursor Maturation and Disposal Is an Early Regulative Mechanism in the Normal Insulin Production of Pancreatic beta-Cells. PLoS One 6(4):e19446. [PubMed: 21559376] [MGI Ref ID J:172346]
Wang J; Osei K. 2011. Proinsulin maturation disorder is a contributor to the defect of subsequent conversion to insulin in beta-cells. Biochem Biophys Res Commun 411(1):150-5. [PubMed: 21723250] [MGI Ref ID J:174771]
Wang J; Takeuchi T; Tanaka S; Kubo SK; Kayo T; Lu D; Takata K; Koizumi A; Izumi T. 1999. A mutation in the insulin 2 gene induces diabetes with severe pancreatic beta-cell dysfunction in the Mody mouse. J Clin Invest 103(1):27-37. [PubMed: 9884331] [MGI Ref ID J:51935]
Wang L; Tang Y; Eisner W; Sparks MA; Buckley AF; Spurney RF. 2014. Augmenting podocyte injury promotes advanced diabetic kidney disease in Akita mice. Biochem Biophys Res Commun 444(4):622-7. [PubMed: 24491571] [MGI Ref ID J:218580]
Wang Q; Frolova AI; Purcell S; Adastra K; Schoeller E; Chi MM; Schedl T; Moley KH. 2010. Mitochondrial dysfunction and apoptosis in cumulus cells of type I diabetic mice. PLoS One 5(12):e15901. [PubMed: 21209947] [MGI Ref ID J:168309]
Wang Y; Zhao X; Shi D; Chen P; Yu Y; Yang L; Xie L. 2013. Overexpression of SIRT1 promotes high glucose-attenuated corneal epithelial wound healing via p53 regulation of the IGFBP3/IGF-1R/AKT pathway. Invest Ophthalmol Vis Sci 54(5):3806-14. [PubMed: 23661372] [MGI Ref ID J:215435]
Wende AR; Soto J; Olsen CD; Pires KM; Schell JC; Larrieu-Lahargue F; Litwin SE; Kakoki M; Takahashi N; Smithies O; Abel ED. 2010. Loss of Bradykinin Signaling Does Not Accelerate the Development of Cardiac Dysfunction in Type 1 Diabetic Akita Mice. Endocrinology :. [PubMed: 20501666] [MGI Ref ID J:161074]
Winnay JN; Dirice E; Liew CW; Kulkarni RN; Kahn CR. 2014. p85alpha deficiency protects beta-cells from endoplasmic reticulum stress-induced apoptosis. Proc Natl Acad Sci U S A 111(3):1192-7. [PubMed: 24395790] [MGI Ref ID J:206472]
Wong DW; Oudit GY; Reich H; Kassiri Z; Zhou J; Liu QC; Backx PH; Penninger JM; Herzenberg AM; Scholey JW. 2007. Loss of angiotensin-converting enzyme-2 (Ace2) accelerates diabetic kidney injury. Am J Pathol 171(2):438-51. [PubMed: 17600118] [MGI Ref ID J:123932]
Wright WS; Yadav AS; McElhatten RM; Harris NR. 2012. Retinal blood flow abnormalities following six months of hyperglycemia in the Ins2(Akita) mouse. Exp Eye Res 98:9-15. [PubMed: 22440813] [MGI Ref ID J:196847]
Yamaguchi K; Takeda K; Kadowaki H; Ueda I; Namba Y; Ouchi Y; Nishitoh H; Ichijo H. 2013. Involvement of ASK1-p38 pathway in the pathogenesis of diabetes triggered by pancreatic ss cell exhaustion. Biochim Biophys Acta 1830(6):3656-63. [PubMed: 23416061] [MGI Ref ID J:202436]
Yamaguchi S; Ishihara H; Yamada T; Tamura A; Usui M; Tominaga R; Munakata Y; Satake C; Katagiri H; Tashiro F; Aburatani H; Tsukiyama-Kohara K; Miyazaki J; Sonenberg N; Oka Y. 2008. ATF4-mediated induction of 4E-BP1 contributes to pancreatic beta cell survival under endoplasmic reticulum stress. Cell Metab 7(3):269-76. [PubMed: 18316032] [MGI Ref ID J:133217]
Yao Y; Jumabay M; Ly A; Radparvar M; Cubberly MR; Bostrom KI. 2013. A role for the endothelium in vascular calcification. Circ Res 113(5):495-504. [PubMed: 23852538] [MGI Ref ID J:213371]
Yeh CK; Harris SE; Mohan S; Horn D; Fajardo R; Chun YH; Jorgensen J; Macdougall M; Abboud-Werner S. 2012. Hyperglycemia and xerostomia are key determinants of tooth decay in type 1 diabetic mice. Lab Invest 92(6):868-82. [PubMed: 22449801] [MGI Ref ID J:184712]
Yoshioka M; Kayo T; Ikeda T; Koizumi A. 1997. A novel locus, Mody4, distal to D7Mit189 on chromosome 7 determines early-onset NIDDM in nonobese C57BL/6 (Akita) mutant mice. Diabetes 46(5):887-94. [PubMed: 9133560] [MGI Ref ID J:40063]
Yu L; Su Y; Paueksakon P; Cheng H; Chen X; Wang H; Harris RC; Zent R; Pozzi A. 2012. Integrin alpha1/Akita double-knockout mice on a Balb/c background develop advanced features of human diabetic nephropathy. Kidney Int 81(11):1086-97. [PubMed: 22297672] [MGI Ref ID J:198186]
Yuan Q; Tang W; Zhang X; Hinson JA; Liu C; Osei K; Wang J. 2012. Proinsulin atypical maturation and disposal induces extensive defects in mouse Ins2+/Akita beta-cells. PLoS One 7(4):e35098. [PubMed: 22509386] [MGI Ref ID J:187092]
Zhou C; Pridgen B; King N; Xu J; Breslow JL. 2011. Hyperglycemic Ins2AkitaLdlr-/- mice show severely elevated lipid levels and increased atherosclerosis: a model of type 1 diabetic macrovascular disease. J Lipid Res 52(8):1483-93. [PubMed: 21606463] [MGI Ref ID J:174983]
Zito E; Chin KT; Blais J; Harding HP; Ron D. 2010. ERO1-beta, a pancreas-specific disulfide oxidase, promotes insulin biogenesis and glucose homeostasis. J Cell Biol 188(6):821-32. [PubMed: 20308425] [MGI Ref ID J:158805]
Zou MH; Li H; He C; Lin M; Lyons TJ; Xie Z. 2011. Tyrosine nitration of prostacyclin synthase is associated with enhanced retinal cell apoptosis in diabetes. Am J Pathol 179(6):2835-44. [PubMed: 22015457] [MGI Ref ID J:180271]
Zuber C; Fan JY; Guhl B; Roth J. 2004. Misfolded proinsulin accumulates in expanded pre-Golgi intermediates and endoplasmic reticulum subdomains in pancreatic beta cells of Akita mice. FASEB J 18(7):917-9. [PubMed: 15033933] [MGI Ref ID J:118471]
de Preux Charles AS; Verdier V; Zenker J; Peter B; Medard JJ; Kuntzer T; Beckmann JS; Bergmann S; Chrast R. 2010. Global transcriptional programs in peripheral nerve endoneurium and DRG are resistant to the onset of type 1 diabetic neuropathy in Ins2 mice. PLoS One 5(5):e10832. [PubMed: 20520806] [MGI Ref ID J:160899]
Animal Health ReportsProduction of mice from cryopreserved embryos or sperm occurs in a maximum barrier room, G200.
Colony Maintenance
Breeding & Husbandry Using heterozygous mutant females for breeding can program diabetes/insulin resistance and confound the diabetic phenotype in the heterozygous mutant progeny. The breeding colony is currently maintained through mating wild-type female with a heterozygous male.
After diabetes onset cages become very wet, due to diabetes-associated polyuria, the health of the heterozygous mutant is best maintained by housing them in cages containing a mixture of regular litter and Alpha-Dri or corn cob bedding, changed minimally twice a week.
|Pricing for USA, Canada and Mexico shipping destinations
Cryopreserved Mice - Ready for Recovery
Animals Provided
Price (US dollars $) Cryorecovery* $2625.00
At least two mice that carry the mutation (if it is a mutant strain) will be provided. Their genotypes may not reflect those discussed in the strain description. Please inquire for possible genotypes and see additional details below.
Frozen Products
Price (US dollars $) Frozen Embryo $1725.00
Standard Supply
Cryopreserved. Ready for recovery. Please refer to pricing and supply notes on the strain data sheet for further information.
Supply Notes
- Available USA, Canada and Mexico shipping destinations
Cryopreserved Embryos
This strain is also available as cryopreserved embryos1. Orders for cryopreserved embryos may be placed with our Customer Service Department. Experienced technicians at The Jackson Laboratory have recovered frozen embryos of this strain successfully. We will provide you enough embryos to perform two embryo transfers. The Jackson Laboratory does not guarantee successful recovery at your facility. For complete information on purchasing embryos, please visit our Cryopreserved Embryos web page.
1 Embryos for most strains are cryopreserved at the two cell stage while some strains are cryopreserved at the eight cell stage. If this information is important to you, please contact Customer Service.
For USA, Canada and Mexico Shipping destinations:
Cryorecovery - Standard.
Progeny testing is not required.
The average number of mice provided from recovery of our cryopreserved strains is 10. The total number of animals provided, their gender and genotype will vary. We will fulfill your order by providing at least two pair of mice, at least one animal of each pair carrying the mutation of interest. Please inquire if larger numbers of animals with specific genotype and genders are needed. Animals typically ship between 10 and 14 weeks from the date of your order. If a second cryorecovery is needed in order to provide the minimum number of animals, animals will ship within 25 weeks. IMPORTANT NOTE: The genotypes of animals provided may not reflect the mating scheme utilized by The Jackson Laboratory prior to cryopreservation, or that discussed in the strain description. Please inquire about possible genotypes which will be recovered for this specific strain. The Jackson Laboratory cannot guarantee the reproductive success of mice shipped to your facility. If the mice are lost after the first three days (post-arrival) or do not produce progeny at your facility, a new order and fee will be necessary.
Cryorecovery to establish a Dedicated Supply for greater quantities of mice. Mice recovered can be used to establish a dedicated colony to contractually supply you mice according to your requirements. Price by quotation. For more information on Dedicated Supply, please contact JAX® Services, Tel: 1-800-422-6423 (from U.S.A., Canada or Puerto Rico only) or 1-207-288-5845 (from any location).
|Pricing for International shipping destinations
Cryopreserved Mice - Ready for Recovery
Animals Provided
Price (US dollars $) Cryorecovery* $3412.50
At least two mice that carry the mutation (if it is a mutant strain) will be provided. Their genotypes may not reflect those discussed in the strain description. Please inquire for possible genotypes and see additional details below.
Frozen Products
Price (US dollars $) Frozen Embryo $2242.50
Standard Supply
Cryopreserved. Ready for recovery. Please refer to pricing and supply notes on the strain data sheet for further information.
Cryopreserved. Ready for recovery. Please refer to pricing and supply notes on the strain data sheet for further information.
|Wild-type from the colony
|Considerations for Choosing Controls
|Control Pricing Information for Genetically Engineered Mutant Strains.
In case of dissatisfaction for a valid reason and claimed in writing by a purchaser within ninety (90) days of receipt of mice, products or services, JACKSON will, at its option, provide credit or replacement for the mice or product received or the services provided.
In no event shall JACKSON, its trustees, directors, officers, employees, and affiliates be liable for any causes of action or damages, including any direct, indirect, special, or consequential damages, arising out of the provision of MICE, PRODUCTS or services, including economic damage or injury to property and lost profits, and including any damage arising from acts or negligence on the part of JACKSON, its agents or employees. Unless prohibited by law, in purchasing or receiving MICE, PRODUCTS or services from JACKSON, purchaser or recipient, or any party claiming by or through them, expressly releases and discharges JACKSON from all such causes of action or damages, and further agrees to defend and indemnify JACKSON from any costs or damages arising out of any third party claims.
MICE and PRODUCTS are to be used in a safe manner and in accordance with all applicable governmental rules and regulations.
The foregoing represents the General Terms and Conditions applicable to JACKSON's MICE, PRODUCTS or services. In addition, special terms and conditions of sale of certain MICE, PRODUCTS or services may be set forth separately in JACKSON web pages, catalogs, price lists, contracts, and/or other documents, and these special terms and conditions shall also govern the sale of these MICE, PRODUCTS and services by JACKSON, and by its licensees and distributors.
Acceptance of delivery of MICE, PRODUCTS or services shall be deemed agreement to these terms and conditions. No purchase order or other document transmitted by purchaser or recipient that may modify the terms and conditions hereof, shall be in any way binding on JACKSON, and instead the terms and conditions set forth herein, including any special terms and conditions set forth separately, shall govern the sale of MICE, PRODUCTS or services by JACKSON.


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The contents of the fountain has inspired a question that's been making the rounds through the WoW community: If you had a coin in that fountain, what would it say? What wish or musing would be left on it? I posed the question to the WoW Insider team to see what they would come up with, ranging from the silly to the serious, from speaking in-character to speaking as a player. Here's what they (we) had to say...
Adam Holisky:
- My Alliance Warrior: "What part of 'follow my target' came out in Orcish?"
- My Alliance Shaman: "That Hunter gear looks so nice..."
- My Priest's coin would say something like, "I wish I could have done more."
- My coin? "Why won't Mike take me to prom?"
Daniel Whitcomb: My in-character wishes...
- My Human Death Knight: "Remember."
- My Night Elf Druid: "I wish to go home."
- My Dwarven Hunter: "I'm doing pretty good. Ain't got much to wish for. Maybe a new hunting rifle?"
- My Human Warlock: "I wish for knowledge and power. Not necessarily in that order."
Manda Miller:
- My Hunter would wish to be loved.
- My Holy Paladin would wish for the ability to break curses, to finally learn the multi-layered mysteries of The Knife, and for everyone else with her hairstyle to suddenly go bald.
- My Death Knight would wish for the Holy Paladin's raid slot.
Matthew Rossi:
- My Tauren Warrior would wish for a sandwich. You can have a sandwich too.
- My Human Warrior would wish to understand why he should do less damage with two huge maces each the size of his entire body than a Rogue does with a couple of daggers.
- My Draenei Shaman would wish for a hat he could wear visibly.
- My Orc Shaman would wish for me to hurry up and get him to 80. And a hat he could wear visibly.
Just like the coins in-game, our responses varied pretty wildly. A few serious wishes (Sylvanas, Tirion), a few silly wishes (Archimonde, Danath), and the occassional shattered 4th wall (Arthas, Anduin). Now I pass the question on to all of you. What would your coin say? Would you (or your character) have a deep and meaningful message within that fountain, or would it be something a little more light-hearted?


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Duo making headlines
HUNTINGTON — A pair of boys basketball players who will be joining the Huntington Prep team for the 2013-14 season are making headlines nationally and internationally for their performances this summer.
Point guard Josh Perkins and small forward Jalen Lindsey have both said they are coming to play for the Huntington Prep Express next season and with them, they bring a big-time game and a big-time list of schools wanting to host them in college.
Perkins, a 6-foot-3 point guard from Denver, Colo., is ranked as the No. 24 player in the Class of 2014 by ESPN and has turned up his value this summer, starting with the Pangos All-American Camp when he went toe-to-toe with Emmanuel Mudiay — one of the top prospects in the Class of 2014.
Last week, Perkins' stock continued to ascend as he was named as the best passer in the NBPA Top 100 camp, a prestigious event put on by former NBA coach John Lucas featuring the nation's best players.
Perkins' offer sheet is long, with scholarship offers from nearly 20 schools including Kansas, Gonzaga, UConn, UCLA and USC. There is also mutual high interest from Kentucky and Syracuse, but offers have not been made.
While Perkins has been tearing up the national scene over the past few weeks, Lindsey has also been making national and even international headlines.
Lindsey, a 6-7 forward from Franklin, Tenn., is ranked No. 32 in ESPN's Top 100 for the Class of 2014, and played well at the Pangos All-American Camp, scoring 28 points in his first two games.
He came to Huntington in May for the signing of Andrew Wiggins, who he will replace at the small forward position for the Express.
Lindsey averaged 19.3 points and 7.9 rebounds last season for Christ Presbyterian, but decided to come to Huntington Prep to elevate his game and take on more of the nation's top players.
Neither player has set a timetable for college commitment, but they are expected to trim their recruiting lists down prior to their August arrival in Huntington.


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Contains printable coloring pages, interactive games, and an array of activities for children.
Features online activities and information about New Year's history and customs.
Contains free online jigsaw puzzles, wallpaper and e-cards. Also offers printable stationery and ideas for making calendars.
Features an archive of interactive games and activities as well as a list of recipes to prepare for parties.
Provides ideas and instructions for New Year's crafts which include cards, calendars and more.
Explores the origin of the holiday and how it is observed and celebrated before and today.
Includes history of this special day, customs, decoration and party ideas, gift traditions, printable cards, and wallpapers.
Resource for information on the origin and various traditions and celebrations of the holiday being observed by countries all across the globe.
Contains printable coloring pages and interactive games and activities for kids.


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Griffin MicConnect lets your XLR microphone make sweet music on your iPhone or iPad
Let's say you have an amazing XLR mic on your big, beefy studio or home recording rig, but you also have an iPad or iPhone and you really want to get that same XLR quality on your way more mobile recording rig, what do you do? Griffin's answer, shown off at CES 2013, is the XLR MicConnect.
The MicConnect supplies phantom power, thanks to AA batteries, and connects via the 3.5mm headphone jack on your iPad or iPad.
I really like the idea of these kinds of accessories, and being able to get the quality on the go that I'm used to at home. If you use an XLR mic, let me know if you're also interested in trying this out.
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Reader comments
Griffin MicConnect lets your XLR microphone make sweet music on your iPhone or iPad
I am extremely interested in setting aside time to try one of these out. As an audio engineer myself, I am always interested in reviewing anything mobile..considering mobile is a big part of our lives (humans, not audio engineers). I will gladly write a review, and yes as jimoro says, "the recorded signal will be limited by the phone's preamp."
And may I also add that (i know i know) my car does not have an aux-in, so I use the Monster iCarPlay cassette deck connection. The audio quality from the headphone jack in my iPod classic is extremely superior to the headphone jack of my iPhone 4S. A difference of about 10dB output, with noticeably lower low frequencies hidden from playback through the iPhone.
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|SOM's Bill Baker to Receive Highest Honor from The Institution of Structural Engineers
|Sunday, 28 February 2010 10:04
William F. Baker P.E., S.E., FIStructE, Structural Engineering Partner at Skidmore, Owings & Merrill LLP (SOM) will be recognized with the Gold Medal from The Institution of Structural Engineers (IStructE) for his work as an internationally acclaimed structural engineer. Founded in 1908 and headquartered in the United Kingdom, IStructE is the world's largest membership organization dedicated to the art and science of structural engineering.
In response to receiving the news, Baker commented, "I am quite overwhelmed by the honor of receiving the Gold Medal. I am humbled to be recognized by my peers and to be in the company of some of the greatest structural engineers of the modern age."
The Gold Medal is the Institution's highest individual award for 'exceptional and outstanding contributions to the advancement of structural engineering.' The award was first presented in 1922 to Professor Henry Adams. Previous winners of the Gold Medal include Felix Candela (1960), Luigi Nervi (1967), Ove Arup (1973), Fritz Leonhardt (1975), Jorg Schlaich (1990), Edmund Happold (1991), Anthony Hunt (1994), Michel Virlogeux (1996), Ian Liddell (1999), Leslie Robertson (2004) and David Nethercot (2009).
Throughout his distinguished career, Baker has dedicated himself to structural innovation – most notably in the design of tall buildings. His most recent contribution has been to develop the "buttressed core" structural system for the Burj Khalifa, a system which, in conjunction with sophisticated wind engineering, makes it possible to construct skyscrapers of extreme elevation. The Burj Khalifa is currently the world's tallest manmade structure.
According to the Council on Tall Buildings and Urban Habitat (CTBUH), three of the five tallest buildings to top out in 2009 are credited to SOM where Baker led the structural engineering: Burj Khalifa (Dubai), Nanjing Greenland Financial Center (Nanjing), and Trump International Hotel & Tower (Chicago).
Other notable projects include the Broadgate Exchange House (London), Korean Air Lines Operations Center (Seoul) Infinity Tower (Dubai), General Motors Renaissance Center – North Lobby (Detroit) and Raspberry Island – Schubert Club Band Shell (St. Paul).
In 2008, Baker received the Fazlur Rahman Khan Medal for lifetime achievement from the Council on Tall Buildings and Urban Habitat. In 2009, he was the first American to receive the Fritz Leonhardt Prize (Germany) in recognition of his engineering accomplishments.
Baker will give his Gold Medal Address at the Institution of Structural Engineers/IABSE Lecture on Thursday, May 13, 2010 at the Institute of Directors, London.
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