BIOC 454 Lecture Notes - Lecture 12: Telomere, H2Afx, Research In Computational Molecular Biology
16 Jan 2018
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Document Summary
Dna damage comes from multiple sources: endogenous sources (inside cells, exogenous sources: chemicals, radiation, etc. replication errors (also an endogenous source) which have escaped the editing process during dna synthesis. Ex: sunburn caused by skin cell apoptosis is regarded as a protective mechanism against uv- induced neoplastic transformation: cellular senescence shares the same reasons, though bacteria can stop growing, it is not same as cellular senescence. Dna damage responses have evolved to respond to dna damage: dna repair, cell cycle checkpoint control: arrests cell cycle progression to allow for repair of dna damage; prevents. There are 6 main mechanisms of dna repair: 1- base excision repair (ber): endogenous (or spontaneous) dna lesions. 2- nucleotide excision repair (ner): important in removal of wide spectrum of damage, especially bulky. 3- mismatch repair: corrects mismatched bases, small deletions an small insertions that result from errors of replicative dna polymerases. 4- recombination repair (homology dependent repair): double strand breaks.
