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What is All of the following are inhibitors of cell cycle except: (PGI Dec 2007) and explain in detail?
Ans D "CDK2 is not inhibitor of cell cycle (it is Cydin-Dependent Kinases). It forms a complex with cyclin E in late Gl, which is involved in the G,/S transition. It also forms a complex with cyclin at the S phse that facilitates the G2/M transition"- Bobbin's 7th/292Cell Cycle inhibitors: Two Main Classes# Cip/Kip family: p21, p27 & P57They block the cell cycle by binding to cyclin - CDK complex.P21 is induced by the tumour suppressor P53.P27 responds to growth suppression such as transforming growth factor beta.# INK4 / APFfamily: p16 INK4A ; p14 ARF.P16 INK4a binds to cyclin D i.e. CDK4 and promotes inhibitory affect of RB.P14 ARF increases p53 level by inhibiting MDM_ activity.Table (Robbins 7th /292) : Main Cell - Cycle Components and their InhibitorsCell-Cycle ComponentMain FunctionCyclin-Dependent KinasesCDK 4Forms a complex with cyclin D. The complex phosphorates RB, allowing the cell to progress through the G1 restriction pointCDK 2Forms a complex with cydin E in late G1, which is involved in the G1/S transition. Forms a complex with cyclin A at the S phse that facilitates the G2/M transitionCDK1Forms a complex with cyclin B, which acts on G2/M transition.InhibitorsCip/Kip family: p21, p27Block the cell cycle by binding to cyclin-CDK complexes. P21 is induced by the tunor suppressor p53. P 27 responds to growth suppressors such as transforming growth factor-b1NK4/ARF . family: p161NK4A, p14ARFP 161Nk4a binds to cyclin D-CDK4 and promotes the inhibitory effects of RB. pl4 ARF increases p53 levels by inhibiting M DM2 activity.Check Componentsp53QTumor suppressor altered in the majority of cancers; causes cell-cycle arrest and apoptosis.Acts mainly through pil to cause cell-cycle arrest. Causes apoptosis by indudg the transcription of pro-apoptotic genes such as BAX. Levels of p53 are negatively regulated by MDM2 through a feedback loop. PS3 is required for the GJS checkpoint and is a main component of the G2/M checkpointAtaxia-telen- giectasia mutated (ATM) 9Activated by mechanisms that sense double stranded DNA breaks. Tmasmits signals to arrest the cell cycle after DNA damage. Acts through p53 in the Gl/S checkpont. At the G2/M checkpoint, it acts both through p53-dependent mechanisms and throgh the inactivation of CDC25 phosphatase, which disrupts the cyclin B-CDK1 complex. Component of a network of genes that include BRCA1 and BRCA2, which link DNA damage with cell-cycle arrest and apoptosis.