BIO 201 Lecture Notes - Lecture 26: Tumor Suppressor Gene, Restriction Point, E2F
18 Apr 2017
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Document Summary
G1/s is the restriction point: point of no return for proliferation. When checkpoints fail it can lead to excessive proliferation of cells. Main causes: mutations such as tumor suppressor genes and proto- oncogenes ex: ras. Tumor suppressor genes: genes whose normal protein products act to prevent cell cycle progression. Loss of function mutations inactivate protein, causing progression through cell cycle at inappropriate times. Prevents cells from entering s phase (g1/s checkpoint) Unstimulated binding to transcription factor e2f preventing transcription of s-phase. Growth factor: activation of ras, transcription of s-phase cyclin, cdk phosphorylates rb, rb falls off e2f. Rb mutations: prevent rb from binding to e2f, growth factor independent activation of e2f, e2f constitutively active, uncontrolled proliferation. Mutations or deletion in p53 gene in ~50% of all human cancers stops cell cycle at g1/s and g2/m checkpoints if dna damage is detected. P53 stops cell cycle if dna is damaged.
