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    MSH2 mismatch repair ATPase MSH2 [ Saccharomyces cerevisiae S288C ]

    Gene ID: 854063, updated on 4-Jan-2025

    GeneRIFs: Gene References Into Functions

    GeneRIFPubMed TitleDate
    Elevated MSH2 MSH3 expression interferes with DNA metabolism in vivo.

    Elevated MSH2 MSH3 expression interferes with DNA metabolism in vivo.
    Medina-Rivera M, Phelps S, Sridharan M, Becker J, Lamb NA, Kumar C, Sutton MD, Bielinsky A, Balakrishnan L, Surtees JA., Free PMC Article

    12/20/2023
    MutSalpha deficiency increases tolerance to DNA damage in yeast lacking postreplication repair.

    MutSα deficiency increases tolerance to DNA damage in yeast lacking postreplication repair.
    Berg IL, Persson JO, Åström SU.

    03/13/2021
    Results provide evidence that the MSH2 gene encoding one of the crucial components of the mismatch repair, is required for transcriptional repression at silent mating-type loci and telomeres.

    Yeast mismatch repair components are required for stable inheritance of gene silencing.
    Liu Q, Zhu X, Lindström M, Shi Y, Zheng J, Hao X, Gustafsson CM, Liu B., Free PMC Article

    08/1/2020
    Msh2-Msh6 Recognizes Mismatched DNA Base Pairs with Different Affinities. Msh2-Msh6 Binding Affects Mismatched Base Pair Dynamics.

    Mismatch Recognition by Saccharomyces cerevisiae Msh2-Msh6: Role of Structure and Dynamics.
    Li Y, Lombardo Z, Joshi M, Hingorani MM, Mukerji I., Free PMC Article

    01/25/2020
    The mutant Msh2-Msh6 complexes exhibited normal mispair recognition and were proficient at recruiting the MMR endonuclease Mlh1-Pms1 to mispaired DNA.

    The properties of Msh2-Msh6 ATP binding mutants suggest a signal amplification mechanism in DNA mismatch repair.
    Graham WJ 5th, Putnam CD, Kolodner RD., Free PMC Article

    06/29/2019
    MSH2 overexpression affected the integrity of the DNA replication fork, causing genome instability phenotypes.

    Genomic Instability Promoted by Overexpression of Mismatch Repair Factors in Yeast: A Model for Understanding Cancer Progression.
    Chakraborty U, Dinh TA, Alani E., Free PMC Article

    10/6/2018
    Msh2-Msh3 hops over nucleosomes and other protein roadblocks, but maintains sufficient contact with DNA to recognize a single lesion. Msh2-Msh6 slides without hopping and is largely blocked by protein roadblocks.

    Dynamic DNA binding licenses a repair factor to bypass roadblocks in search of DNA lesions.
    Brown MW, Kim Y, Williams GM, Huck JD, Surtees JA, Finkelstein IJ., Free PMC Article

    07/2/2016
    By detecting Pol2 and Msh2 dynamics within the same strain, we established that the mismatch recognition complex binds origins and spreads to adjacent regions with the replisome.

    The Eukaryotic Mismatch Recognition Complexes Track with the Replisome during DNA Synthesis.
    Haye JE, Gammie AE., Free PMC Article

    06/4/2016
    Data suggest that bot hATP and structure-specific repair substrates cooperate to direct Msh2-Msh3-mediated repair and provide an explanation for the msh3Y942A separation-of-function phenotype.

    ATP binding and hydrolysis by Saccharomyces cerevisiae Msh2-Msh3 are differentially modulated by mismatch and double-strand break repair DNA substrates.
    Kumar C, Eichmiller R, Wang B, Williams GM, Bianco PR, Surtees JA., Free PMC Article

    01/10/2015
    Msh2-Msh6 localizes PCNA to repair sites after mispair recognition.

    PCNA and Msh2-Msh6 activate an Mlh1-Pms1 endonuclease pathway required for Exo1-independent mismatch repair.
    Goellner EM, Smith CE, Campbell CS, Hombauer H, Desai A, Putnam CD, Kolodner RD., Free PMC Article

    10/18/2014
    a comparative study of Msh2-Msh3 and Msh2-Msh6 for mispair binding, sliding clamp formation, and Mlh1-Pms1 recruitment

    Mispair-specific recruitment of the Mlh1-Pms1 complex identifies repair substrates of the Saccharomyces cerevisiae Msh2-Msh3 complex.
    Srivatsan A, Bowen N, Kolodner RD., Free PMC Article

    05/24/2014
    Mlh1-Mlh3, a meiotic crossover and DNA mismatch repair factor, is a Msh2-Msh3-stimulated endonuclease.

    Mlh1-Mlh3, a meiotic crossover and DNA mismatch repair factor, is a Msh2-Msh3-stimulated endonuclease.
    Rogacheva MV, Manhart CM, Chen C, Guarne A, Surtees J, Alani E., Free PMC Article

    04/26/2014
    Disruption of cell-cycle elements upstream of MSH2 results in a defect in mismatch repair.DNA damaging agents incresase Msh2 turnover.

    Cell-cycle and DNA damage regulation of the DNA mismatch repair protein Msh2 occurs at the transcriptional and post-transcriptional level.
    Tennen RI, Haye JE, Wijayatilake HD, Arlow T, Ponzio D, Gammie AE., Free PMC Article

    06/22/2013
    Msh2-Msh3 directly interferes with normal Okazaki fragment processing by flap endonuclease1 (Rad27) and DNA ligase I (Cdc9) in the presence of TNR sequences, thereby producing small, incremental expansion events

    Msh2-Msh3 interferes with Okazaki fragment processing to promote trinucleotide repeat expansions.
    Kantartzis A, Williams GM, Balakrishnan L, Roberts RL, Surtees JA, Bambara RA., Free PMC Article

    03/2/2013
    Data suggest that recognition of small insertion/deletion mispairs by Msh3, but not Msh2, requires more interaction with DNA conformations induced by small insertion/deletion mispairs than induced by large that are bent and strand separated.

    Functional studies and homology modeling of Msh2-Msh3 predict that mispair recognition involves DNA bending and strand separation.
    Dowen JM, Putnam CD, Kolodner RD., Free PMC Article

    07/26/2010
    analysis of the interaction between the Msh2 and Msh6 nucleotide-binding sites in the Saccharomyces cerevisiae Msh2-Msh6 complex

    Interaction between the Msh2 and Msh6 nucleotide-binding sites in the Saccharomyces cerevisiae Msh2-Msh6 complex.
    Hargreaves VV, Shell SS, Mazur DJ, Hess MT, Kolodner RD., Free PMC Article

    04/19/2010
    Msh2 plays multiple roles in the formation of chromosomal translocations following acute levels of DNA damage

    Msh2 blocks an alternative mechanism for non-homologous tail removal during single-strand annealing in Saccharomyces cerevisiae.
    Manthey GM, Naik N, Bailis AM., Free PMC Article

    03/15/2010
    results suggest that MSH2-MSH6 binding to homoduplex regions of DNA recruits NHP6A, which then prevents further binding of MSH2-MSH6 to these sites unless a mismatch is present.

    Modulation of the DNA-binding activity of Saccharomyces cerevisiae MSH2-MSH6 complex by the high-mobility group protein NHP6A, in vitro.
    Labazi M, Jaafar L, Flores-Rozas H., Free PMC Article

    02/15/2010
    Interactions between Msh2-Msh6 and DNA are dominated by lateral movement of the protein along the helical axis and have implications for how MutS family members travel along DNA at different stages of the mismatch repair reaction.

    Dynamic basis for one-dimensional DNA scanning by the mismatch repair complex Msh2-Msh6.
    Gorman J, Chowdhury A, Surtees JA, Shimada J, Reichman DR, Alani E, Greene EC., Free PMC Article

    01/21/2010
    communication between the mispair-binding domain and the ATPase domain is conserved between Msh2-Msh3 and Msh2-Msh6

    Chimeric Saccharomyces cerevisiae Msh6 protein with an Msh3 mispair-binding domain combines properties of both proteins.
    Shell SS, Putnam CD, Kolodner RD., Free PMC Article

    01/21/2010
    MSH2 acts in repair of base pair mismatch.

    Saccharomyces cerevisiae Msh2-Msh3 acts in repair of base-base mispairs.
    Harrington JM, Kolodner RD., Free PMC Article

    01/21/2010
    The binding of MSH2-MSH3 to mismatch DNA involves protein-DNA contacts that appear very different from those required for MSH2-MSH6 mismatch binding.

    Saccharomyces cerevisiae MSH2-MSH3 and MSH2-MSH6 complexes display distinct requirements for DNA binding domain I in mismatch recognition.
    Lee SD, Surtees JA, Alani E., Free PMC Article

    01/21/2010
    genetic analysis of the interaction between the Saccharomyces cerevisiae MSH2-MSH6 and MLH1-PMS1 complexes with DNA

    Analysis of the interaction between the Saccharomyces cerevisiae MSH2-MSH6 and MLH1-PMS1 complexes with DNA using a reversible DNA end-blocking system.
    Mendillo ML, Mazur DJ, Kolodner RD.

    01/21/2010
    MSH2-MSH3 binding to its substrates creates a unique nucleoprotein structure that may signal downstream steps in repair that include interactions with mismatch repair (MMR) and nucleotide excision repair factors.

    Mismatch repair factor MSH2-MSH3 binds and alters the conformation of branched DNA structures predicted to form during genetic recombination.
    Surtees JA, Alani E.

    01/21/2010
    Either Msh2p/Mlh1p-independent mispair removal leads to restoration of one of the markers flanking the double strand breaks.

    MLH1 and MSH2 promote the symmetry of double-strand break repair events at the HIS4 hotspot in Saccharomyces cerevisiae.
    Hoffmann ER, Eriksson E, Herbert BJ, Borts RH., Free PMC Article

    01/21/2010
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