Bloom syndrome cells undergo p53-dependent apoptosis and delayed assembly of BRCA1 and NBS1 repair complexes at stalled replication forks. - Wikidata - wikimedia - TriplyDB

Bloom syndrome cells undergo p53-dependent apoptosis and delayed assembly of BRCA1 and NBS1 repair complexes at stalled replication forks.

Bloom syndrome cells undergo p53-dependent apoptosis and delayed assembly of BRCA1 and NBS1 repair complexes at stalled replication forks.

http://www.wikidata.org/entity/Q36325528

about

BLAP75, an essential component of Bloom's syndrome protein complexes that maintain genome integrity POT1 stimulates RecQ helicases WRN and BLM to unwind telomeric DNA substrates Telomere dysfunction and cell survival: roles for distinct TIN2-containing complexes Chk1 and p21 cooperate to prevent apoptosis during DNA replication fork stress Physical and functional interaction between the Bloom's syndrome gene product and the largest subunit of chromatin assembly factor 1 BLAP18/RMI2, a novel OB-fold-containing protein, is an essential component of the Bloom helicase-double Holliday junction dissolvasome Functional interaction between BLM helicase and 53BP1 in a Chk1-mediated pathway during S-phase arrest Disease-causing missense mutations in human DNA helicase disorders The role of RecQ helicases in non-homologous end-joining An N-terminal acidic region of Sgs1 interacts with Rpa70 and recruits Rad53 kinase to stalled forks.The broken genome: genetic and pharmacologic approaches to breaking DNA Association of BLM and BRCA1 during Telomere Maintenance in ALT Cells Unwinding protein complexes in ALTernative telomere maintenance.SUMO modification regulates BLM and RAD51 interaction at damaged replication forks.Werner syndrome protein associates with gamma H2AX in a manner that depends upon Nbs1.RecQ helicases: guardian angels of the DNA replication fork.Analysis of the DNA binding activity of BRCA1 and its modulation by the tumour suppressor p53.Human RPA phosphorylation by ATR stimulates DNA synthesis and prevents ssDNA accumulation during DNA-replication stress The Werner syndrome protein suppresses telomeric instability caused by chromium (VI) induced DNA replication stress.Phosphorylation of BLM, dissociation from topoisomerase IIIalpha, and colocalization with gamma-H2AX after topoisomerase I-induced replication damage.The role of post-translational modifications in fine-tuning BLM helicase function during DNA repair Junction of RecQ helicase biochemistry and human disease.Time to bloom.Tumor suppressor p53 represses transcription of RECQ4 helicase.Werner protein protects nonproliferating cells from oxidative DNA damage Collaboration of Werner syndrome protein and BRCA1 in cellular responses to DNA interstrand cross-links.Helicase-inactivating mutations as a basis for dominant negative phenotypes.Damaged mitochondria in Fanconi anemia - an isolated event or a general phenomenon?BLM SUMOylation regulates ssDNA accumulation at stalled replication forks.The DNA repair endonuclease XPG interacts directly and functionally with the WRN helicase defective in Werner syndrome Critical interaction domains between bloom syndrome protein and RAD51 RMI1 promotes DNA replication fork progression and recovery from replication fork stress Combined modalities of resistance in an oxaliplatin-resistant human gastric cancer cell line with enhanced sensitivity to 5-fluorouracil.p53-dependent release of Alarmin HMGB1 is a central mediator of senescent phenotypes The Werner syndrome protein functions in repair of Cr(VI)-induced replication-associated DNA damage.Genomic instability resulting from Blm deficiency compromises development, maintenance, and function of the B cell lineage.Analysis of alternative lengthening of telomere markers in BRCA1 defective cells.Smc5/6-mediated regulation of replication progression contributes to chromosome assembly during mitosis in human cells.RecQ family members combine strand pairing and unwinding activities to catalyze strand exchange.Chromosome breakage is regulated by the interaction of the BLM helicase and topoisomerase IIalpha.

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Bloom syndrome cells undergo p53-dependent apoptosis and delayed assembly of BRCA1 and NBS1 repair complexes at stalled replication forks.

http://www.wikidata.org/entity/Q36325528

description

2003 nî lūn-bûn

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2003年の論文

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2003年学术文章

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2003年学术文章

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2003年學術文章

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2003年學術文章

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2003年學術文章

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Albert R Davalos

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Judith Campisi

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P2860

TIN2, a new regulator of telomere length in human cells

Nuclear structure in normal and Bloom syndrome cells

Regulation and localization of the Bloom syndrome protein in response to DNA damage

TANK2, a new TRF1-associated poly(ADP-ribose) polymerase, causes rapid induction of cell death upon overexpression

p53 has a direct apoptogenic role at the mitochondria

NBS1 localizes to gamma-H2AX foci through interaction with the FHA/BRCT domain

Bloom's and Werner's syndrome genes suppress hyperrecombination in yeast sgs1 mutant: implication for genomic instability in human diseases

Extension of life-span by introduction of telomerase into normal human cells

BASC, a super complex of BRCA1-associated proteins involved in the recognition and repair of aberrant DNA structures

Bloom's syndrome. I. Genetical and clinical observations in the first twenty-seven patients

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1197-1209

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10.1083/JCB.200304016

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