Termination of translesion DNA synthesis

Stable Identifier
R-HSA-5656169
Type
Pathway
Species
Homo sapiens
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5/5
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The initiation and extent of translesion DNA synthesis (TLS) has to be tightly controlled in order to limit TLS-induced mutagenesis, caused by the low fidelity of TLS-participating DNA polymerases. Since monoubiquitination of PCNA at lysine residue K164 is a prerequisite for the assembly of TLS complexes on damaged DNA templates, PCNA deubiquitination is a key step in TLS termination that allows DNA polymerase switching from Y family DNA polymerases involved in TLS to replicative DNA polymerases delta and epsilon (Povlsen et al. 2012, Park et al. 2014).
Literature References
PubMed ID Title Journal Year
23000965 Systems-wide analysis of ubiquitylation dynamics reveals a key role for PAF15 ubiquitylation in DNA-damage bypass

Nielsen, ML, Poulsen, SL, Sylvestersen, KB, Beli, P, Choudhary, C, Povlsen, LK, Bekker-Jensen, S, Mailand, N, Poulsen, JW, Wagner, SA

Nat. Cell Biol. 2012
24768535 Modification of PCNA by ISG15 plays a crucial role in termination of error-prone translesion DNA synthesis

Lee, SW, Seol, JH, Yang, SW, Yu, KR, Park, JM, Ka, SH, Jeon, YJ, Chung, CH

Mol. Cell 2014
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