ATR functions as a gene dosage-dependent tumor suppressor on a mismatch repair-deficient background - Wikidata - awgldk - TriplyDB

ATR functions as a gene dosage-dependent tumor suppressor on a mismatch repair-deficient background

ATR functions as a gene dosage-dependent tumor suppressor on a mismatch repair-deficient background

http://www.wikidata.org/entity/Q28274709

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Mutation analysis of the ATR gene in breast and ovarian cancer families.Trial Watch: Targeting ATM-CHK2 and ATR-CHK1 pathways for anticancer therapy Cell-cycle checkpoints and cancer DNA damage response genes and the development of cancer metastasis ATR: an essential regulator of genome integrity BRIT1 regulates early DNA damage response, chromosomal integrity, and cancer Combining ATR suppression with oncogenic Ras synergistically increases genomic instability, causing synthetic lethality or tumorigenesis in a dosage-dependent manner.Histone modifiers in cancer: friends or foes?Analysis of mutations that dissociate G(2) and essential S phase functions of human ataxia telangiectasia-mutated and Rad3-related (ATR) protein kinase.Oncogenic stress sensitizes murine cancers to hypomorphic suppression of ATR Genome maintenance defects in cultured cells and mice following partial inactivation of the essential cell cycle checkpoint gene Hus1.Germline mutation in ATR in autosomal- dominant oropharyngeal cancer syndrome.DNA damage response curtails detrimental replication stress and chromosomal instability induced by the dietary carcinogen PhIP.Tumor suppressor genetics.Structure and function of the components of the human DNA mismatch repair system.The ATR barrier to replication-born DNA damage.ATR signalling: more than meeting at the fork.Haploinsufficiency of DNA Damage Response Genes and their Potential Influence in Human Genomic Disorders.Monoallelic loss of tumor suppressor GRIM-19 promotes tumorigenesis in mice.Reduced ATR or Chk1 expression leads to chromosome instability and chemosensitization of mismatch repair-deficient colorectal cancer cells.Deficiencies in Chfr and Mlh1 synergistically enhance tumor susceptibility in mice.Is activation of the intra-S checkpoint in human fibroblasts an important factor in protection against UV-induced mutagenesis?Ligand modulation of a dinuclear platinum compound leads to mechanistic differences in cell cycle progression and arrest Safeguarding genome integrity: the checkpoint kinases ATR, CHK1 and WEE1 restrain CDK activity during normal DNA replication.Haploinsufficiency in mouse models of DNA repair deficiency: modifiers of penetrance.Selective tumor killing based on specific DNA-damage response deficiencies.Charity begins at home: non-coding RNA functions in DNA repair Impact of Age and Insulin-Like Growth Factor-1 on DNA Damage Responses in UV-Irradiated Human Skin.Decatenation checkpoint-defective melanomas are dependent on PI3K for survival.A majority of human melanoma cell lines exhibits an S phase-specific defect in excision of UV-induced DNA photoproducts.Increased replication initiation and conflicts with transcription underlie Cyclin E-induced replication stress.Autoregulatory mechanisms of phosphorylation of checkpoint kinase 1.The DNA damage checkpoint pathway promotes extensive resection and nucleotide synthesis to facilitate homologous recombination repair and genome stability in fission yeast.MLH1 deficiency enhances tumor cell sensitivity to ganciclovir.Cellular and clinical impact of haploinsufficiency for genes involved in ATR signaling.Disparate roles of ATR and ATM in immunoglobulin class switch recombination and somatic hypermutation Haploinsufficiency of Tumor Suppressor Genes is Driven by the Cumulative Effect of microRNAs, microRNA Binding Site Polymorphisms and microRNA Polymorphisms: An In silico Approach.ATR and H2AX cooperate in maintaining genome stability under replication stress.Insulin-like Growth Factor 1 Receptor Signaling Is Required for Optimal ATR-CHK1 Kinase Signaling in Ultraviolet B (UVB)-irradiated Human Keratinocytes.ATR inhibition preferentially targets homologous recombination-deficient tumor cells.

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ATR functions as a gene dosage-dependent tumor suppressor on a mismatch repair-deficient background

http://www.wikidata.org/entity/Q28274709

description

2004 nî lūn-bûn

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2004 թուականի Օգոստոսին հրատարակուած գիտական յօդուած

@hyw

2004 թվականի օգոստոսին 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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name

ATR functions as a gene dosage ...... ch repair-deficient background

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ATR functions as a gene dosage ...... ch repair-deficient background

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ATR functions as a gene dosage ...... ch repair-deficient background

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type

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ATR functions as a gene dosage ...... ch repair-deficient background

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ATR functions as a gene dosage ...... ch repair-deficient background

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ATR functions as a gene dosage ...... ch repair-deficient background

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prefLabel

ATR functions as a gene dosage ...... ch repair-deficient background

@ast

ATR functions as a gene dosage ...... ch repair-deficient background

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ATR functions as a gene dosage ...... ch repair-deficient background

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SJ.EMBOJ.7600315

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The EMBO Journal

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ATR functions as a gene dosage ...... ch repair-deficient background

@en

P2093

Barbara K Goodman

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

Carlos A Tirado

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

Cheng-Chung Tsao

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

Robert T Abraham

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

Ryohei Furumai

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

Xiao-Fan Wang

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Yanan Fang

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

P2860

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

Mutations of mitotic checkpoint genes in human cancers

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

The role of chromosomal instability in tumor initiation.

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

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

Mutation of a mutL homolog in hereditary colon cancer

Genetic instabilities in human cancers

Targeted disruption of the cell-cycle checkpoint gene ATR leads to early embryonic lethality in mice

A splicing mutation affecting expression of ataxia-telangiectasia and Rad3-related protein (ATR) results in Seckel syndrome

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10.1038/SJ.EMBOJ.7600315

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15

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23

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2004-08-04T00:00:00Z

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8426483

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15282542

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514932

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