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

Loss of ATM kinase activity leads to embryonic lethality in mice.

The Journal of cell biology - 6 Aug 2012

Daniel Jeremy A, Pellegrini Manuela, Lee Baeck-Seung, Guo Zhi, Filsuf Darius, Belkina Natalya V, You Zhongsheng, Paull Tanya T, Sleckman Barry P, Feigenbaum Lionel, Nussenzweig André

Abstract excerpt

Ataxia telangiectasia (A-T) mutated (ATM) is a key deoxyribonucleic acid (DNA) damage signaling kinase that regulates DNA repair, cell cycle checkpoints, and apoptosis. The majority of patients with A-T, a cancer-prone neurodegenerative disease, present with null mutations in Atm. To determine whether the functions of ATM are mediated solely by its kinase activity, we generated two mouse models containing single,...

Read the complete abstract on PubMed

Topics

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

Share to Ataxia Telangiectasia Mutated Proteins
Share to B-Lymphocytes

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Catalysis

Share to Gene Expression Regulation, Enzymologic

Share to Genomic Instability

Share to Neurodegenerative Diseases

Share to Poly(ADP-ribose) Polymerases

Share to Tumor Suppressor Proteins

Source

Open in PubMed Open full text

Identifiers

PMID: 22869595
DOI: 10.1083/jcb.201204035
PMCID: PMC3413361

Genes

ATM

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 2 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Loss of ATM kinase activity leads to embryonic lethality in mice.PMID 22869595Read ↗

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

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

ATM Kinase Dead: From Ataxia Telangiectasia Syndrome to CancerSemantic proximity Read ↗

Ataxia‐telangiectasia, cancer and the pathobiology of the <i>ATM</i> geneSemantic proximity Read ↗

Inactive Atm abrogates DSB repair in mouse cerebellum more than does Atm loss, without causing a neurological phenotypeSemantic proximity Read ↗

The versatile functions of ATM kinaseSemantic proximity Read ↗

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

The Cancer-Associated ATM R3008H Mutation Reveals the Link between ATM Activation and Its Exchange.Semantic proximity Read ↗

Functional consequences of sequence alterations in the ATM gene.Semantic proximity Read ↗

A novel mouse model for ataxia-telangiectasia with a N-terminal mutation displays a behavioral defect and a low incidence of lymphoma but no increased oxidative burden.Semantic proximity Read ↗

The ATM protein: the importance of being active.Semantic proximity Read ↗

The ATM signaling network in development and diseaseSemantic proximity Read ↗

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