ArticleNucleic acids research2002
Human DNA polymerase mu (Pol mu) exhibits an unusual replication slippage ability at AAF lesion.
Article in Nucleic acids research, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 24 citations in OpenAlex.
- The molecular basis and disease relevance of non-homologous DNA end joining.Nature reviews. Molecular cell biology · 2020Review
- Mechanistic Basis for the Bypass of a Bulky DNA Adduct Catalyzed by a Y-Family DNA Polymerase.Journal of the American Chemical Society · 2015Article
- Translesion DNA synthesis and mutagenesis in eukaryotes.Cold Spring Harbor perspectives in biology · 2013Review
- DNA expansions generated by human Polμ on iterative sequences.Nucleic acids research · 2013Article
- Kinetic analysis of the bypass of a bulky DNA lesion catalyzed by human Y-family DNA polymerases.Chemical research in toxicology · 2012Article
- Base excision repair: contribution to tumorigenesis and target in anticancer treatment paradigms.Current medicinal chemistry · 2012Review
- Polymerases in nonhomologous end joining: building a bridge over broken chromosomes.Antioxidants & redox signaling · 2011Review
- DNA pol λ's extraordinary ability to stabilize misaligned DNA.Journal of the American Chemical Society · 2010Article
- Conferring a template-dependent polymerase activity to terminal deoxynucleotidyltransferase by mutations in the Loop1 region.Nucleic acids research · 2009Article
- Mechanistic studies of the bypass of a bulky single-base lesion catalyzed by a Y-family DNA polymerase.The Journal of biological chemistry · 2009Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
We analyzed the ability of various cell extracts to extend a radiolabeled primer past an N-2-acetylaminofluorene (AAF) adduct located on a primed single-stranded template. When the 3' end of the primer is located opposite the lesion, partially fractionated human primary fibroblast extracts efficiently catalyzed primer-terminus extension by adding a ladder of about 15 dGMPs, in an apparently non-templated reaction. This activity was not detected in SV40-transformed fibroblasts or in HeLa cell extracts unless purified human DNA polymerase mu (Pol mu) was added. In contrast, purified human Pol mu alone could only add three dGMPs as predicted from the sequence of the template. These results suggest that a cofactor(s) present in cellular extracts modifies Pol mu activity. The production of the dGMP ladder at the primer terminus located opposite the AAF adduct reveals an unusual ability of Pol mu (in conjunction with its cofactor) to perform DNA synthesis from a slipped intermediate containing several unpaired bases.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.