Mismatch repair-dependent G2 checkpoint induced by low doses of SN1 type methylating agents requires the ATR kinase. - Wikidata - awgldk - TriplyDB

Mismatch repair-dependent G2 checkpoint induced by low doses of SN1 type methylating agents requires the ATR kinase.

Mismatch repair-dependent G2 checkpoint induced by low doses of SN1 type methylating agents requires the ATR kinase.

http://www.wikidata.org/entity/Q31070565

about

ATR kinase activation mediated by MutSalpha and MutLalpha in response to cytotoxic O6-methylguanine adducts The histone mark H3K36me3 regulates human DNA mismatch repair through its interaction with MutSα Methylator-induced, mismatch repair-dependent G2 arrest is activated through Chk1 and Chk2 DNA mismatch repair: molecular mechanism, cancer, and ageing The accumulation of MMS-induced single strand breaks in G1 phase is recombinogenic in DNA polymerase beta defective mammalian cells Characterization of the interactome of the human MutL homologues MLH1, PMS1, and PMS2 Structural, molecular and cellular functions of MSH2 and MSH6 during DNA mismatch repair, damage signaling and other noncanonical activities Early Chk1 phosphorylation is driven by temozolomide-induced, DNA double strand break- and mismatch repair-independent DNA damage N-nitroso-N-ethylurea activates DNA damage surveillance pathways and induces transformation in mammalian cells.Treatment of pituitary carcinomas and atypical pituitary adenomas: a review HIV-1 Vpr-induced apoptosis is cell cycle dependent and requires Bax but not ANT Anti-proliferative activity of the quassinoid NBT-272 in childhood medulloblastoma cells Human MLH1 protein participates in genomic damage checkpoint signaling in response to DNA interstrand crosslinks, while MSH2 functions in DNA repair A new isoquinolinium derivative, Cadein1, preferentially induces apoptosis in p53-defective cancer cells with functional mismatch repair via a p38-dependent pathway.Residual gammaH2AX foci as an indication of lethal DNA lesions.Embryonic lethality after combined inactivation of Fancd2 and Mlh1 in mice.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.E1B and E4 oncoproteins of adenovirus antagonize the effect of apoptosis inducing factor The mismatch repair system modulates curcumin sensitivity through induction of DNA strand breaks and activation of G2-M checkpoint.Mismatch repair proteins are activators of toxic responses to chromium-DNA damage.Histone/protein deacetylase SIRT1 is an anticancer therapeutic target.Interaction between human mismatch repair recognition proteins and checkpoint sensor Rad9-Rad1-Hus1 Genomic and epigenetic instability in colorectal cancer pathogenesis.ASCIZ regulates lesion-specific Rad51 focus formation and apoptosis after methylating DNA damage.HOXA10 is associated with temozolomide resistance through regulation of the homologous recombinant DNA repair pathway in glioblastoma cell lines.Genotype to phenotype: analyzing the effects of inherited mutations in colorectal cancer families.Targeting and processing of site-specific DNA interstrand crosslinks.Loss of DNA mismatch repair imparts a selective advantage in planarian adult stem cells.Human pluripotent stem cells have a novel mismatch repair-dependent damage response.Lynch syndrome-associated mutations in MSH2 alter DNA repair and checkpoint response functions in vivo.The Rad50S allele promotes ATM-dependent DNA damage responses and suppresses ATM deficiency: implications for the Mre11 complex as a DNA damage sensor.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.Surgical resection of malignant gliomas-role in optimizing patient outcome.Phosphorylated hMSH6: DNA mismatch versus DNA damage recognition.Thiopurines in current medical practice: molecular mechanisms and contributions to therapy-related cancer.Major differences between tumor and normal human cell fates after exposure to chemotherapeutic monofunctional alkylator Therapeutic modulation of epigenetic drivers of drug resistance in ovarian cancer.DNA mismatch repair proteins are required for efficient herpes simplex virus 1 replication

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P2860

Mismatch repair-dependent G2 checkpoint induced by low doses of SN1 type methylating agents requires the ATR kinase.

http://www.wikidata.org/entity/Q31070565

description

2004 nî lūn-bûn

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2004 թուականի Յունիսին հրատարակուած գիտական յօդուած

@hyw

2004 թվականի հունիսին հրատարակված գիտական հոդված

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2004年の論文

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2004年論文

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2004年論文

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2004年論文

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2004年論文

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2004年論文

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2004年论文

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name

Mismatch repair-dependent G2 c ...... gents requires the ATR kinase.

@ast

Mismatch repair-dependent G2 c ...... gents requires the ATR kinase.

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type

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Mismatch repair-dependent G2 c ...... gents requires the ATR kinase.

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Mismatch repair-dependent G2 c ...... gents requires the ATR kinase.

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prefLabel

Mismatch repair-dependent G2 c ...... gents requires the ATR kinase.

@ast

Mismatch repair-dependent G2 c ...... gents requires the ATR kinase.

@en

P1433

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Genes & Development

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Mismatch repair-dependent G2 c ...... gents requires the ATR kinase.

@en

P2093

Giancarlo Marra

http://www.w3.org/2001/XMLSchema#string

Josef Jiricny

http://www.w3.org/2001/XMLSchema#string

Massimiliano Di Pietro

http://www.w3.org/2001/XMLSchema#string

Nina Mojas

http://www.w3.org/2001/XMLSchema#string

Petr Cejka

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P2860

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

Mitotic phosphorylation of histone H3: spatio-temporal regulation by mammalian Aurora kinases

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

hMSH3 and hMSH6 interact with PCNA and colocalize with it to replication foci

Chk1 is an essential kinase that is regulated by Atr and required for the G(2)/M DNA damage checkpoint

Essential and dispensable roles of ATR in cell cycle arrest and genome maintenance

Megabase chromatin domains involved in DNA double-strand breaks in vivo

Sensing DNA damage through ATRIP recognition of RPA-ssDNA complexes

Caffeine abolishes the mammalian G(2)/M DNA damage checkpoint by inhibiting ataxia-telangiectasia-mutated kinase activity

A critical role for histone H2AX in recruitment of repair factors to nuclear foci after DNA damage

P304

1331-1344

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scholarly article

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10.1101/GAD.294404

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11

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18

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Stefano Ferrari

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2004-06-01T00:00:00Z

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8532092

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15175264

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420358

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