Molecules and Cells

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Fig. 1.

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Fig. 1. p53-dependent DNA damage response and the Fanconi anemia (FA) pathway. (A) p53-dependent pathway. DNA damage activates ATR/ATM and CHK1/CHK2 kinases leading to p53 phosphorylation. p53 undergoes p300 dependent acetylation which transactivates specific p53 target genes resulting in either cell cycle arrest and DNA repair or apoptosis. (B) FA pathway. The FA pathway is activated during the S-phase of the cell cycle upon DNA replication fork stalling at ICLs. ATR/CHK1 is activated and in turn activates FA core complex, which promotes the monoubiquitylation of the FANCI-FANCD2 heterodimer. The ubiquitylated FANCD2-FANCI heterodimer at ICLs recruits DNA repair proteins involved in nucleotide excision repair, translesion synthesis and homologous recombination to stabilize the fork and repair ICLs.
Mol. Cells 2020;43:99~106 https://doi.org/10.14348/molcells.2019.0304
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