Discover Community Create You

Loading publication...

Noodle always counts identifier-free feature events for service operation. With your permission, Google Analytics can also estimate audience and engagement. Search text, publication identifiers, cookies, IP addresses and browser fingerprints are never included in Noodle's first-party event counters.

Privacy details

Article

Functional Link between BLM Defective in Bloom's Syndrome and the Ataxia-telangiectasia-mutated Protein, ATM

1 Aug 2002

Abstract excerpt

Chromosome aberrations, genomic instability, and cancer predisposition are hallmarks of a number of syndromes in which the defective genes recognize and/or repair DNA damage or are involved in some aspect of DNA processing. We report here direct interaction between BLM, mutated in Bloom's Syndrome (BS), and ATM, mutated is ataxia-telangiectasia, and we have mapped the sites of interaction. Full-length BLM cDNA...

Read the complete abstract on PubMed

Topics

Share this publication in a Topic to start or enrich a Post.

Share to Cancer-related Molecular Pathways
Share to Carcinogens and Genotoxicity Assessment
Share to DNA Repair Mechanisms

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Source

Identifiers

PMID: 12034743
DOI: 10.1074/jbc.m203801200

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Functional Link between BLM Defective in Bloom's Syndrome and the Ataxia-telangiectasia-mutated Protein, ATMPMID 12034743Read ↗

Functional interactions between BLM and XRCC3 in the cell.Semantic proximity Read ↗

Disruption of the BLM gene in ATM-null DT40 cells does not exacerbate either phenotype.Semantic proximity Read ↗

Bloom syndrome radials are predominantly non-homologous and are suppressed by phosphorylated BLM.Semantic proximity Read ↗

Bloom's syndrome protein is required for correct relocalization of RAD50/MRE11/NBS1 complex after replication fork arrestSemantic proximity Read ↗

Absence of BLM leads to accumulation of chromosomal DNA breaks during both unperturbed and disrupted S phasesSemantic proximity Read ↗

TopBP1 interacts with BLM to maintain genome stability but is dispensable for preventing BLM degradation.Semantic proximity Read ↗

Evidence for BLM and Topoisomerase IIIalpha interaction in genomic stability.Semantic proximity Read ↗

Regulation and Localization of the Bloom Syndrome Protein in Response to DNA DamageSemantic proximity Read ↗

Functional interaction between BLM helicase and 53BP1 in a Chk1-mediated pathway during S-phase arrestSemantic proximity Read ↗

ATM-dependent phosphorylation and accumulation of endogenous BLM protein in response to ionizing radiationSemantic proximity Read ↗

Intra-nuclear trafficking of the BLM helicase to DNA damage-induced foci is regulated by SUMO modification.Semantic proximity Read ↗

Phosphorylation of the Bloom's syndrome helicase and its role in recovery from S-phase arrest.Semantic proximity Read ↗

⌁Select a neighboring publication to make it the new centre.