Phosphorylation of mismatch repair proteins MSH2 and MSH6 affecting MutSalpha mismatch-binding activity.
about
Transcriptional regulation of human DNA repair genes following genotoxic stress: trigger mechanisms, inducible responses and genotoxic adaptationStructural, molecular and cellular functions of MSH2 and MSH6 during DNA mismatch repair, damage signaling and other noncanonical activitiesOpposing regulatory roles of phosphorylation and acetylation in DNA mispair processing by thymine DNA glycosylaseHistone deacetylase 10 regulates DNA mismatch repair and may involve the deacetylation of MutS homolog 2.Gene expression profiling of naïve sheep genetically resistant and susceptible to gastrointestinal nematodes.The oncogenic phosphatase WIP1 negatively regulates nucleotide excision repairCooperative nuclear localization sequences lend a novel role to the N-terminal region of MSH6.Loss of the mismatch repair protein MSH6 in human glioblastomas is associated with tumor progression during temozolomide treatment.Phosphorylated hMSH6: DNA mismatch versus DNA damage recognition.Adaptive upregulation of DNA repair genes following benzo(a)pyrene diol epoxide protects against cell death at the expense of mutations.Fusion tyrosine kinase NPM-ALK Deregulates MSH2 and suppresses DNA mismatch repair function novel insights into a potent oncoproteinInterplay between mismatch repair and chromatin assemblyExonuclease 1 (Exo1) is required for activating response to S(N)1 DNA methylating agents.Structure and function of the components of the human DNA mismatch repair system.Overexpression of MutSα Complex Proteins Predicts Poor Prognosis in Oral Squamous Cell Carcinoma.WRN protects against topo I but not topo II inhibitors by preventing DNA break formationc-Fos is required for excision repair of UV-light induced DNA lesions by triggering the re-synthesis of XPFRevealing protein networks and gene-drug connectivity in cancer from direct information.NPM-ALK mediates phosphorylation of MSH2 at tyrosine 238, creating a functional deficiency in MSH2 and the loss of mismatch repair.Delayed c-Fos activation in human cells triggers XPF induction and an adaptive response to UVC-induced DNA damage and cytotoxicity.Three prime exonuclease I (TREX1) is Fos/AP-1 regulated by genotoxic stress and protects against ultraviolet light and benzo(a)pyrene-induced DNA damage.hMSH2 expression is driven by AP1-dependent regulation through phorbol-ester exposure.Atypical protein kinase C stimulates nucleotide excision repair activity.Degadration of mismatch repair hMutSalpha heterodimer by the ubiquitin-proteasome pathway.Defective human MutY phosphorylation exists in colorectal cancer cell lines with wild-type MutY alleles.Phosphorylation-dependent signaling controls degradation of DNA mismatch repair protein PMS2.
P2860
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P2860
Phosphorylation of mismatch repair proteins MSH2 and MSH6 affecting MutSalpha mismatch-binding activity.
description
2002 nî lūn-bûn
@nan
2002年の論文
@ja
2002年論文
@yue
2002年論文
@zh-hant
2002年論文
@zh-hk
2002年論文
@zh-mo
2002年論文
@zh-tw
2002年论文
@wuu
2002年论文
@zh
2002年论文
@zh-cn
name
Phosphorylation of mismatch re ...... pha mismatch-binding activity.
@en
Phosphorylation of mismatch re ...... pha mismatch-binding activity.
@nl
type
label
Phosphorylation of mismatch re ...... pha mismatch-binding activity.
@en
Phosphorylation of mismatch re ...... pha mismatch-binding activity.
@nl
prefLabel
Phosphorylation of mismatch re ...... pha mismatch-binding activity.
@en
Phosphorylation of mismatch re ...... pha mismatch-binding activity.
@nl
P2093
P2860
P356
P1476
Phosphorylation of mismatch re ...... pha mismatch-binding activity.
@en
P2093
Bernd Kaina
Maja T Tomicic
Markus Christmann
P2860
P304
P356
10.1093/NAR/30.9.1959
P407
P577
2002-05-01T00:00:00Z