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 p53-mediated DNA damage response to ionizing radiation in fibroblasts from ataxia-without-telangiectasia patients.

International journal of radiation biology - 1 Sept 1998

Jongmans W, Vuillaume M, Kleijer W J, Lakin N D, Hall J

Abstract excerpt

PURPOSE: To assess the functionality of the p53-mediated pathway, activated by the ataxia-telangiectasia gene product (ATM) in response to ionizing radiation, in cells derived from four ataxia-without-telangiectasia patients. These patients exhibit cerebellar ataxia and cellular abnormalities that are compatible with the diagnosis of ataxia-telangiectasia (AT), but the telangiectasias normally seen in AT patients...

Read the complete abstract on PubMed

Topics

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

Share to Proteins
Share to Blotting, Northern
Share to Cells, Cultured

Methodology Data sources Editorial policy Privacy Delete account & data About Contact Helena Bioinformatics

Share to DNA-Binding Proteins

Share to Gene Expression

Share to Mutation

Share to Phenotype

Share to RNA, Messenger

Source

Identifiers

PMID: 9737532
DOI: 10.1080/095530098141438

Genes

ATM

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-08.1.

Source receipt: pubmed, retrieved 7 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence. Graph snapshot: 2026-09-29.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

The p53-mediated DNA damage response to ionizing radiation in fibroblasts from ataxia-without-telangiectasia patients.PMID 9737532Read ↗

ATM: the protein encoded by the gene mutated in the radiosensitive syndrome ataxia-telangiectasia.Semantic proximity Read ↗

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

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

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

Reduced induction of P53 protein by gamma-irradiation in ataxia telangiectasia cells without constitutional mutations in exons 5, 6, 7, and 8 of the p53 gene.Semantic proximity Read ↗

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

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

Molecular perspectives on cancer, the cell cycle and the inherited disorder ataxia-telangiectasia.Semantic proximity Read ↗

Ataxia-telangiectasia mutated kinase (ATM) as a central regulator of radiation-induced DNA damage response.Semantic proximity Read ↗

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

ATM&A Key Determinant of Multiple Cellular Responses to IrradiationSemantic proximity Read ↗

Contribution of the Atm Protein to Maintaining Cellular Homeostasis Evidenced by Continuous Activation of the AP-1 Pathway in Atm-deficient BrainsSemantic proximity Read ↗

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