Sister chromatid-based DNA repair is mediated by RAD54, not by DMC1 or TID1.
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Frequent and efficient use of the sister chromatid for DNA double-strand break repair during budding yeast meiosisDifferential contributions of mammalian Rad54 paralogs to recombination, DNA damage repair, and meiosisHuman Rad54B is a double-stranded DNA-dependent ATPase and has biochemical properties different from its structural homolog in yeast, Tid1/Rdh54A role for RAD54B in homologous recombination in human cellsTid1/Rdh54 promotes colocalization of rad51 and dmc1 during meiotic recombinationYeast recombination factor Rdh54 functionally interacts with the Rad51 recombinase and catalyzes Rad51 removal from DNA.Recombination protein Tid1p controls resolution of cohesin-dependent linkages in meiosis in Saccharomyces cerevisiae.Role for the silencing protein Dot1 in meiotic checkpoint control.A role for MMS4 in the processing of recombination intermediates during meiosis in Saccharomyces cerevisiaeMek1 kinase activity functions downstream of RED1 in the regulation of meiotic double strand break repair in budding yeast.Mek1 Down Regulates Rad51 Activity during Yeast Meiosis by Phosphorylation of Hed1Promotion of Rad51-dependent D-loop formation by yeast recombination factor Rdh54/Tid1.The PCNA interaction protein box sequence in Rad54 is an integral part of its ATPase domain and is required for efficient DNA repair and recombinationMouse pachytene checkpoint 2 (trip13) is required for completing meiotic recombination but not synapsisSchizosaccharomyces pombe Rdh54 (TID1) acts with Rhp54 (RAD54) to repair meiotic double-strand breaksRole of RAD52 epistasis group genes in homologous recombination and double-strand break repairHigh copy number suppression of the meiotic arrest caused by a dmc1 mutation: REC114 imposes an early recombination block and RAD54 promotes a DMC1-independent DSB repair pathway.Excess single-stranded DNA inhibits meiotic double-strand break repair.Biochemistry of Meiotic Recombination: Formation, Processing, and Resolution of Recombination Intermediates.Pathways to meiotic recombination in Arabidopsis thaliana.Properties of Mitotic and Meiotic Recombination in the Tandemly-Repeated CUP1 Gene Cluster in the Yeast Saccharomyces cerevisiae.Spontaneous and double-strand break-induced recombination, and gene conversion tract lengths, are differentially affected by overexpression of wild-type or ATPase-defective yeast Rad54.Mek1 suppression of meiotic double-strand break repair is specific to sister chromatids, chromosome autonomous and independent of Rec8 cohesin complexesPartner choice during meiosis is regulated by Hop1-promoted dimerization of Mek1.Distinct P-element excision products in somatic and germline cells of Drosophila melanogaster.The Mus81/Mms4 endonuclease acts independently of double-Holliday junction resolution to promote a distinct subset of crossovers during meiosis in budding yeast.Involvement of the Arabidopsis SWI2/SNF2 chromatin remodeling gene family in DNA damage response and recombination.CTG repeat instability and size variation timing in DNA repair-deficient mice.Unequal sister chromatid and homolog recombination at a tandem duplication of the A1 locus in maize.Rad54: the Swiss Army knife of homologous recombination?Arrest, adaptation, and recovery following a chromosome double-strand break in Saccharomyces cerevisiae.Functions of the Snf2/Swi2 family Rad54 motor protein in homologous recombination.Genetic evidence that synaptonemal complex axial elements govern recombination pathway choice in micePch2 modulates chromatid partner choice during meiotic double-strand break repair in Saccharomyces cerevisiae.HO endonuclease-induced recombination in yeast meiosis resembles Spo11-induced events.Identification of Putative Mek1 Substrates during Meiosis in Saccharomyces cerevisiae Using Quantitative Phosphoproteomics.Homologous recombination and its regulationSaccharomyces cerevisiae Dmc1 and Rad51 proteins preferentially function with Tid1 and Rad54 proteins, respectively, to promote DNA strand invasion during genetic recombination.Predictive models for carcinogenicity and mutagenicity: frameworks, state-of-the-art, and perspectives.Prevention of DNA Rereplication Through a Meiotic Recombination Checkpoint Response.
P2860
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P2860
Sister chromatid-based DNA repair is mediated by RAD54, not by DMC1 or TID1.
description
1999 nî lūn-bûn
@nan
1999年の論文
@ja
1999年論文
@yue
1999年論文
@zh-hant
1999年論文
@zh-hk
1999年論文
@zh-mo
1999年論文
@zh-tw
1999年论文
@wuu
1999年论文
@zh
1999年论文
@zh-cn
name
Sister chromatid-based DNA repair is mediated by RAD54, not by DMC1 or TID1.
@en
type
label
Sister chromatid-based DNA repair is mediated by RAD54, not by DMC1 or TID1.
@en
prefLabel
Sister chromatid-based DNA repair is mediated by RAD54, not by DMC1 or TID1.
@en
P2093
P2860
P356
P1433
P1476
Sister chromatid-based DNA repair is mediated by RAD54, not by DMC1 or TID1.
@en
P2093
P2860
P304
P356
10.1093/EMBOJ/18.9.2648
P407
P577
1999-05-01T00:00:00Z