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Translesion DNA synthesis: structure and specificity (236.3)
Author(s) -
Aggarwal Aneel
Publication year - 2014
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.28.1_supplement.236.3
Subject(s) - dna polymerase , dna replication , dna , biology , mutagenesis , dna polymerase ii , dna synthesis , dna damage , dna repair , eukaryotic dna replication , primase , polymerase , genetics , microbiology and biotechnology , biochemistry , mutation , gene , polymerase chain reaction , reverse transcriptase
The survival of all organisms depends critically on the ability to faithfully replicate DNA. However, cellular DNA is continually subjected to damaging agents such as sunlight and chemical pollutants externally, and oxidation and hydrolysis internally. The replicative DNA polymerases (Pols) are unable to replicate through these lesions, resulting in the stalling of the replication fork. Whether cells can replicate through DNA lesions has been a key question in the areas of DNA replication, mutagenesis, and carcinogenesis. The answer to this longstanding puzzle has come relatively recently with the discovery of a number of translesion DNA synthesis (TLS) polymerases that are related and belong to the Y‐superfamily. I will present some of our structural studies on TLS DNA polymerases, addressing the basis of their selectivity and ability to bypass to specific DNA lesions.