Endonucleolytic Function of MutLα in Human Mismatch Repair
By F. Kadyrov, L. Dzantiev, N. Constantin, P. Modrich. 2006
581 citations recorded by the source corpus.
Subfields: Molecular Biology, Pathology and Forensic Medicine, Surgery
View Paper: https://www.semanticscholar.org/paper/3633b63e8d1fe649c5bf481ba2475dae290f0c0d
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In Molecular Biology
- Gregory A. Newby
- Britt Adamson
- Mustafa Sahin
- David R. Liu
- Jonathan S. Weissman
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- Lei S. Qi
- Caixia Gao
In Surgery
Citations in the corpus
- Enhanced prime editing systems by manipulating cellular determinants of editing outcomes (2021, methodology): “We co-transfected HEK293T cells with plasmids encoding PE2, pegRNAs, and catalytically impaired mutants of human MSH2, MSH6, PMS2, and MLH1 (Gueneau et al., 2013; Iaccarino et al., 1998; Kadyrov et al., 2006; Räschle et al., 2002; Tomer et al., 2002) (Figures 4A).”
- Mechanisms of DNA damage, repair and mutagenesis (2017, unknown): “MutLa regulates termination of mismatch-provoked excision, and its endonuclease activity plays a role in the 30 nick-directed digestion by EXO1 (Exonuclease 1) in a PCNA/RFC dependent manner [Zhang et al., 2005; Kadyrov et al., 2006].”
- Proliferating cell nuclear antigen (PCNA): a key factor in DNA replication and cell cycle regulation. (2011, unknown): “Recent studies suggest that the recruitment of PCNA, RFC and EXO1 is necessary to activate the latent endonuclease activity of the MutLa complex (MLH1-PMS2; Kadyrov et al., 2006).”
- PCNA, the maestro of the replication fork. (2007, unknown): “However, recent studies indicate that PCNA, RFC, and EXO1 are required to activate a cryptic endonucleolytic activity of the mammalian mediator PMS2, which creates a nick 5′ of the mispair, allowing EXO1 to act in its usual 5′-to-3′ polarity (Kadyrov et al., 2006).”
- Mechanism and regulation of class switch recombination. (2008, background): “Msh2-–Msh6, along with Mlh1-Pms2, recruit Exo1 (and accessory proteins) to a nearby 5′ nick, from where Exo1 begins to excise toward the mismatch (90, 91), creating a DSB with a 5′ single-strand overhang, which can be filled in by DNA polymerase.”