Methylator-induced, mismatch repair-dependent G2 arrest is activated through Chk1 and Chk2 - Test2 - elhamkhani - TriplyDB

Methylator-induced, mismatch repair-dependent G2 arrest is activated through Chk1 and Chk2

Methylator-induced, mismatch repair-dependent G2 arrest is activated through Chk1 and Chk2

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ATR kinase activation mediated by MutSalpha and MutLalpha in response to cytotoxic O6-methylguanine adducts DNA mismatch repair: molecular mechanism, cancer, and ageing Early Chk1 phosphorylation is driven by temozolomide-induced, DNA double strand break- and mismatch repair-independent DNA damage Human MLH1 protein participates in genomic damage checkpoint signaling in response to DNA interstrand crosslinks, while MSH2 functions in DNA repair Nuclear reorganization of DNA mismatch repair proteins in response to DNA damage.Interactions of human mismatch repair proteins MutSalpha and MutLalpha with proteins of the ATR-Chk1 pathway.The mismatch repair system modulates curcumin sensitivity through induction of DNA strand breaks and activation of G2-M checkpoint.Targeting and processing of site-specific DNA interstrand crosslinks.Human pluripotent stem cells have a novel mismatch repair-dependent damage response.Selenium compounds activate ATM-dependent DNA damage response via the mismatch repair protein hMLH1 in colorectal cancer cells.O6-Methylguanine DNA lesions induce an intra-S-phase arrest from which cells exit into apoptosis governed by early and late multi-pathway signaling network activation.DNA damage during reoxygenation elicits a Chk2-dependent checkpoint response ATR-dependent phosphorylation and activation of ATM in response to UV treatment or replication fork stalling.CHK2 kinase in the DNA damage response and beyond Exonuclease 1 (Exo1) is required for activating response to S(N)1 DNA methylating agents.TLR9 engagement on CD4 T lymphocytes represses gamma-radiation-induced apoptosis through activation of checkpoint kinase response elements.Mismatch repair defects and Lynch syndrome: The role of the basic scientist in the battle against cancer DNA mismatch repair and the DNA damage response.Contributions of DNA repair and damage response pathways to the non-linear genotoxic responses of alkylating agents.Bifunctional DNA alkylator 1,3-bis(2-chloroethyl)-1-nitrosourea activates the ATR-Chk1 pathway independently of the mismatch repair pathway.Reduced ATR or Chk1 expression leads to chromosome instability and chemosensitization of mismatch repair-deficient colorectal cancer cells.Oligonucleotide-directed gene-editing technology: mechanisms and future prospects.The transglutaminase 2 gene (TGM2), a potential molecular marker for chemotherapeutic drug sensitivity, is epigenetically silenced in breast cancer.MMR/c-Abl-dependent activation of ING2/p73alpha signaling regulates the cell death response to N-methyl-N'-nitro-N-nitrosoguanidine.NPM-ALK mediates phosphorylation of MSH2 at tyrosine 238, creating a functional deficiency in MSH2 and the loss of mismatch repair.Acidic tumor microenvironment downregulates hMLH1 but does not diminish 5-fluorouracil chemosensitivity.Oxidative DNA damage is involved in ochratoxin A-induced G2 arrest through ataxia telangiectasia-mutated (ATM) pathways in human gastric epithelium GES-1 cells in vitro.MLH1 mediates PARP-dependent cell death in response to the methylating agent N-methyl-N-nitrosourea.Drug-sensitive DNA polymerase δ reveals a role for mismatch repair in checkpoint activation in yeast.Role of c-Abl kinase in DNA mismatch repair-dependent G2 cell cycle checkpoint arrest responses.MLH1- and ATM-dependent MAPK signaling is activated through c-Abl in response to the alkylator N-methyl-N'-nitro-N'-nitrosoguanidine.Zerumbone, a bioactive sesquiterpene, induces G2/M cell cycle arrest and apoptosis in leukemia cells via a Fas- and mitochondria-mediated pathway.Activated neutrophils induce an hMSH2-dependent G2/M checkpoint arrest and replication errors at a (CA)13-repeat in colon epithelial cells.DNA mismatch repair protein Mlh1 is required for tetravalent chromium intermediate-induced DNA damage.

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Methylator-induced, mismatch repair-dependent G2 arrest is activated through Chk1 and Chk2

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2005 nî lūn-bûn

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2005 թուականի Մարտին հրատարակուած գիտական յօդուած

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Methylator-induced, mismatch r ...... ctivated through Chk1 and Chk2

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Methylator-induced, mismatch r ...... ctivated through Chk1 and Chk2

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Methylator-induced, mismatch r ...... ctivated through Chk1 and Chk2

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Methylator-induced, mismatch r ...... ctivated through Chk1 and Chk2

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Methylator-induced, mismatch r ...... ctivated through Chk1 and Chk2

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Methylator-induced, mismatch r ...... ctivated through Chk1 and Chk2

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Methylator-induced, mismatch r ...... ctivated through Chk1 and Chk2

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Methylator-induced, mismatch r ...... ctivated through Chk1 and Chk2

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Methylator-induced, mismatch r ...... ctivated through Chk1 and Chk2

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Molecular Biology of the Cell

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Methylator-induced, mismatch r ...... ctivated through Chk1 and Chk2

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Aaron W Adamson

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Dillon I Beardsley

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Kevin D Brown

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R Baskaran

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Wan-Ju Kim

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Yajuan Gao

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P2860

Linkage of ATM to cell cycle regulation by the Chk2 protein kinase

Overproduction of human Myt1 kinase induces a G2 cell cycle delay by interfering with the intracellular trafficking of Cdc2-cyclin B1 complexes

Involvement of the MKK6-p38gamma cascade in gamma-radiation-induced cell cycle arrest

The ATM-Chk2-Cdc25A checkpoint pathway guards against radioresistant DNA synthesis

MSH2 and ATR form a signaling module and regulate two branches of the damage response to DNA methylation

N-methyl-N'-nitro-N-nitrosoguanidine-induced senescence-like growth arrest in colon cancer cells is associated with loss of adenomatous polyposis coli protein, microtubule organization, and telomeric DNA

Dephosphorylation and activation of a p34cdc2/cyclin B complex in vitro by human CDC25 protein

The mismatch repair system is required for S-phase checkpoint activation

Disruption of the checkpoint kinase 1/cell division cycle 25A pathway abrogates ionizing radiation-induced S and G2 checkpoints.

ATR-mediated checkpoint pathways regulate phosphorylation and activation of human Chk1

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