BIOL3108 Lecture Notes - Lecture 14: Cell Cycle Checkpoint, Myc, Prometaphase

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12 Jan 2020
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Lecture 14: evading growth suppressors (tp53 and cell. Checkpoints key to preventing division of defective genes. Checkpoint defects drive cancer by enabling continued cell cycle and survival of cells with. Most cancers occur in people >50 as time enables multiple mutations to accumulate. Maintain genomic integrity (detect mutations and ensure dna repair and proper chromosome segregation) Encode proteins that turn off cell division and enable cell death when mutations detected in non-cancer cells. Behaves as classic tumour suppressor to inhibit proliferation. Senses dna damage, inhibits cell cycle, initiates dna repair. If dna impossible to repair activates cell death (apoptosis) If it cannot be fixed -> cell death. Tp53 touches all pathways that lead to cancer. Amino-terminal (at) mutations in p53"s transactivation domain or od most frequently only partially reduce transcriptional activity, to maintain tumour suppressor functions. Oligomerization domain (od) mutants sometimes disrupt tetramerizaton to result in complete loss of function. Dna-binding domain (dbd) mutants are at best nonfunctional.

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