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

Upregulation of FasL and apoptosis in thymic lymphomas in Atm knock-in mice.

Toxicology - 27 Dec 2002

Lavin Martin F, Spring Kevin

Abstract excerpt

Several members of the phosphatidylinositol 3-kinase family play key roles in recognising and responding to damage in DNA, induced by a variety of chemicals and other agents. One of these, ATM, the product of the gene mutated in the human genetic disorder ataxia-telangiectasia (A-T), recognises double strand breaks in DNA caused by ionizing radiation and radiomimetic chemicals. In order to study DNA damage...

Read the complete abstract on PubMed

Topics

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

Share to Chromosome Aberrations
Share to Fas Ligand Protein
Share to Genetic Vectors

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Immunoblotting

Share to Lymphoma, T-Cell

Share to Membrane Glycoproteins

Share to Protein Kinases

Share to Up-Regulation

Source

Identifiers

PMID: 12505357
DOI: 10.1016/s0300-483x(02)00462-6

Genes

SRI
ATM

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-07.1.

Source receipt: pubmed, retrieved 7 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Upregulation of FasL and apoptosis in thymic lymphomas in Atm knock-in mice.PMID 12505357Read ↗

Atm knock-in mice harboring an in-frame deletion corresponding to the human ATM 7636del9 common mutation exhibit a variant phenotype.Semantic proximity Read ↗

Atm-deficient mice: a paradigm of ataxia telangiectasia.Semantic proximity Read ↗

Cancer risk and the ATM gene: a continuing debate.Semantic proximity Read ↗

Abnormal development of Purkinje cells and lymphocytes in Atm mutant miceSemantic proximity Read ↗

ATM: from gene to function.Semantic proximity Read ↗

Kinase-dead ATM protein causes genomic instability and early embryonic lethality in mice.Semantic proximity Read ↗

Pleiotropic defects in ataxia-telangiectasia protein-deficient mice.Semantic proximity Read ↗

A new role for ATMSemantic proximity Read ↗

Mice heterozygous for mutation in Atm, the gene involved in ataxia-telangiectasia, have heightened susceptibility to cancer.Semantic proximity Read ↗

Targeting ATM-deficient CLL through interference with DNA repair pathwaysSemantic proximity Read ↗

Ataxia telangiectasia gene mutations in leukaemia and lymphoma.Semantic proximity Read ↗

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

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