Term
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Definition
| CYCLIN-DEPENDENT KINASES: Forms a complex with cyclin D that phosphorylates RB, allowing the cell to progress through the G1 restriction point. |
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Term
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Definition
| CYCLIN-DEPENDENT KINASES: Forms a complex with cyclin E in late G1, which is involved in G1/S transition. Forms a complex with cyclin A at the S phase that facilitates G2/M transition. |
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Term
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Definition
| CYCLIN-DEPENDENT KINASES: Forms a complex with cyclin B that facilitates G2/M transition. |
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Term
| CIP/KIP family: p21, p27 (CDKN2A-C) |
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Definition
| INHIBITORS: Block the cell cycle by binding to cyclin-CDK complexes; p21 is induced by the tumor suppressor p53; p27 responds to growth suppressors such as TGF-beta. |
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Term
| INK4/ARF family (CDKN1A-D) |
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Definition
| INHIBITORS: p16/INK4a binds to cyclin DÐCDK4 and promotes the inhibitory effects of RB; p14/ARF increases p53 levels by inhibiting MDM2 activity. |
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Term
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Definition
| CHECKPOINT COMPONENTS: Tumor suppressor gene altered in the majority of cancers; causes cell cycle arrest and apoptosis. Acts mainly through p21 to cause cell cycle arrest. Causes apoptosis by inducing the transcription of pro-apoptotic genes such as BAX. Levels of p53 are negatively regulated by MDM2 through a feedback loop. p53 is required for the G1/S checkpoint and is a main component of the G2/M checkpoint. |
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Term
| Ataxia-telangiectasia mutated |
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Definition
| CHECKPOINT COMPONENTS: Activated by mechanisms that sense double-stranded DNA breaks. Transmits signals to arrest the cell cycle after DNA damage. Acts through p53 in the G1/S checkpoint. At the G2/M checkpoint, it acts both through p53-dependent mechanisms and through the inactivation of CDC25 phosphatase, which disrupts the cyclin BÐCDK1 complex. Component of a network of genes that include BRCA1 and BRCA2, which link DNA damage with cell cycle arrest and apoptosis. |
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