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

The Ataxia telangiectasia Gene Product Is Required for Oxidative Stress-induced G1 and G2Checkpoint Function in Human Fibroblasts

1 Jun 2001

Abstract excerpt

Ataxia telangiectasia (AT) is an autosomal recessive disorder characterized by neuronal degeneration accompanied by ataxia, telangiectasias, acute cancer predisposition, and sensitivity to ionizing radiation (IR). Cells from individuals with AT show unusual sensitivity to IR, severely attenuated cell cycle checkpoint functions, and poor p53 induction in response to IR compared with normal human fibroblasts...

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: 11290740
DOI: 10.1074/jbc.m011303200

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 4 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

The Ataxia telangiectasia Gene Product Is Required for Oxidative Stress-induced G1 and G2Checkpoint Function in Human FibroblastsPMID 11290740Read ↗

ATM-Dependent and -Independent Gene Expression Changes in Response to Oxidative Stress, Gamma Irradiation, and UV IrradiationSemantic proximity Read ↗

Ataxia-telangiectasia and cellular responses to DNA damage.Semantic proximity Read ↗

Stress-induced Premature Senescence in hTERT-expressing Ataxia Telangiectasia FibroblastsSemantic proximity Read ↗

Endogenously induced DNA double strand breaks arise in heterochromatic DNA regions and require ataxia telangiectasia mutated and Artemis for their repairSemantic proximity Read ↗

Correction of ATM mutations in iPS cells from two ataxia-telangiectasia patients restores DNA damage and oxidative stress responses.Semantic proximity Read ↗

Pathogenesis of ataxia-telangiectasia: the next generation of ATM functionsSemantic proximity Read ↗

ATM: the product of the gene mutated in ataxia-telangiectasia.Semantic proximity Read ↗

Accelerated replicative senescence of ataxia‐telangiectasia skin fibroblasts is retained at physiologic oxygen levels, with unique and common transcriptional patternsSemantic proximity Read ↗

Splitting the ATM: distinct repair and checkpoint defects in ataxia-telangiectasia.Semantic proximity Read ↗

The p53-mediated DNA damage response to ionizing radiation in fibroblasts from ataxia-without-telangiectasia patients.Semantic proximity Read ↗

A Double-Strand Break Repair Defect in ATM-Deficient Cells Contributes to RadiosensitivitySemantic proximity Read ↗

The role of ATM in DNA damage responses and cancer.Semantic proximity Read ↗

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