The many substrates and functions of ATM (Q28205055)

Nature Reviews Molecular Cell Biology

Europe PubMed Central

title

The many substrates and functions of ATM (English)

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author name string

M B Kastan

series ordinal

1

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D S Lim

series ordinal

2

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language of work or name

English

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publication date

December 2000

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published in

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volume

1

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issue

3

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page(s)

179-86

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cites work

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The DNA-dependent protein kinase

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Substrate specificities and identification of putative substrates of ATM kinase family members

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Purification and characterization of ATM from human placenta. A manganese-dependent, wortmannin-sensitive serine/threonine protein kinase

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PI 3-kinase is a dual specificity enzyme: autoregulation by an intrinsic protein-serine kinase activity.

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Purification and DNA binding properties of the ataxia-telangiectasia gene product ATM.

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Characterization of ATM expression, localization, and associated DNA-dependent protein kinase activity

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Murine scid cells complement ataxia-telangiectasia cells and show a normal post-irradiation response of DNA synthesis

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Intact G2-phase checkpoint in cells of a human cell line lacking DNA-dependent protein kinase activity.

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Radiosensitivity in ataxia-telangiectasia: a new explanation

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Radiosensitivity in ataxia-telangiectasia: anomalies in radiation-induced cell cycle delay

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Utilization of oriented peptide libraries to identify substrate motifs selected by ATM.

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The complexity of p53 modulation: emerging patterns from divergent signals

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WAF1, a potential mediator of p53 tumor suppression

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DNA damage-induced phosphorylation of p53 alleviates inhibition by MDM2

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DNA damage induces phosphorylation of the amino terminus of p53

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Regulation of p53 function and stability by phosphorylation

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Phosphorylation of Ser-20 mediates stabilization of human p53 in response to DNA damage

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Serine15 phosphorylation stimulates p53 transactivation but does not directly influence interaction with HDM2.

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DNA damage activates p53 through a phosphorylation-acetylation cascade

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Mdm2 promotes the rapid degradation of p53

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Regulation of p53 stability by Mdm2

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Rapid ATM-dependent phosphorylation of MDM2 precedes p53 accumulation in response to DNA damage

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DNA damage-inducible phosphorylation of p53 at N-terminal sites including a novel site, Ser20, requires tetramerization

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DNA damage-induced activation of p53 by the checkpoint kinase Chk2

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Linkage of ATM to cell cycle regulation by the Chk2 protein kinase

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Caffeine abolishes the mammalian G(2)/M DNA damage checkpoint by inhibiting ataxia-telangiectasia-mutated kinase activity

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p53-dependent G1 arrest involves pRB-related proteins and is disrupted by the human papillomavirus 16 E7 oncoprotein

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DNA damage triggers a prolonged p53-dependent G1 arrest and long-term induction of Cip1 in normal human fibroblasts

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Nibrin, a novel DNA double-strand break repair protein, is mutated in Nijmegen breakage syndrome

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ATM phosphorylates p95/nbs1 in an S-phase checkpoint pathway

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A checkpoint regulates the rate of progression through S phase in S. cerevisiae in response to DNA damage.

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S-phase-specific activation of Cds1 kinase defines a subpathway of the checkpoint response in Schizosaccharomyces pombe

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Essential role of BETA2/NeuroD1 in development of the vestibular and auditory systems

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Control of the DNA damage checkpoint by chk1 and rad53 protein kinases through distinct mechanisms

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Regulation of RAD53 by the ATM-like kinases MEC1 and TEL1 in yeast cell cycle checkpoint pathways

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Centrosome amplification and a defective G2-M cell cycle checkpoint induce genetic instability in BRCA1 exon 11 isoform-deficient cells

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On the nature of a defect in cells from individuals with ataxia-telangiectasia

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Histone H1 dephosphorylation is mediated through a radiation-induced signal transduction pathway dependent on ATM.

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Sensing of ionizing radiation-induced DNA damage by ATM through interaction with histone deacetylase

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DNA double strand break repair in mammalian cells

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High spontaneous intrachromosomal recombination rates in ataxia-telangiectasia

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High frequency and error-prone DNA recombination in ataxia telangiectasia cell lines

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Radiation-induced assembly of Rad51 and Rad52 recombination complex requires ATM and c-Abl

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The controlling role of ATM in homologous recombinational repair of DNA damage

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Association of BRCA1 with Rad51 in mitotic and meiotic cells

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BRCA1 required for transcription-coupled repair of oxidative DNA damage

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Brca1 controls homology-directed DNA repair

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hCds1-mediated phosphorylation of BRCA1 regulates the DNA damage response

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Functional link of BRCA1 and ataxia telangiectasia gene product in DNA damage response

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Defective neurogenesis resulting from DNA ligase IV deficiency requires Atm

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Ataxia telangiectasia mutant protein activates c-Abl tyrosine kinase in response to ionizing radiation

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A novel ionizing radiation-induced signaling pathway that activates the transcription factor NF-kappaB.

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ATM binds to beta-adaptin in cytoplasmic vesicles

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Expression of the ataxia-telangiectasia gene (ATM) product in human cerebellar neurons during development.

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ATM is a cytoplasmic protein in mouse brain required to prevent lysosomal accumulation.

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Participation of ATM in insulin signalling through phosphorylation of eIF-4E-binding protein 1.

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Accessing DNA damage in chromatin: insights from transcription

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A role for ATR in the DNA damage-induced phosphorylation of p53

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TEL1, an S. cerevisiae homolog of the human gene mutated in ataxia telangiectasia, is functionally related to the yeast checkpoint gene MEC1

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The mei-41 gene of D. melanogaster is a structural and functional homolog of the human ataxia telangiectasia gene

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cDNA cloning and gene mapping of a candidate human cell cycle checkpoint protein

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Ataxia telangiectasia-mutated phosphorylates Chk2 in vivo and in vitro

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Identifiers

DOI

10.1038/35043058

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Consolidated OpenCitations Corpus – April 2017

Dimensions Publication ID

3643233

1037972283

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Fatcat ID

release_qx4cukni7zf2rfwaynjl6lxjne

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Fatcat

https://api.fatcat.wiki/v0/release/qx4cukni7zf2rfwaynjl6lxjne

24 November 2022

mapped directly with Wikidata item

3643233

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Consolidated OpenCitations Corpus – April 2017

Consolidated OpenCitations Corpus – April 2017

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