Functional link between BLM defective in Bloom's syndrome and the ataxia-telangiectasia-mutated protein, ATM (Q28201174)

1

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Padmini Kedar

2

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Hideo Kaneko

3

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Philip Chen

4

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Toshiyuki Fukao

5

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Cheng Peng

6

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Sergei Beresten

7

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Nuri Gueven

8

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David Purdie

9

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Susan Lees-Miller

10

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Nathan Ellis

11

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Naomi Kondo

12

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Martin F Lavin

Journal of Biological Chemistry

13

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language of work or name

English

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publication date

23 August 2002

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published in

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volume

277

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page(s)

30515-23

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issue

34

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cites work

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rqh1+, a fission yeast gene related to the Bloom's and Werner's syndrome genes, is required for reversible S phase arrest

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The Bloom's syndrome gene product is a 3'-5' DNA helicase

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The DNA helicase activity of BLM is necessary for the correction of the genomic instability of bloom syndrome cells

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Cell cycle regulation of the endogenous wild type Bloom's syndrome DNA helicase

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Possible association of BLM in decreasing DNA double strand breaks during DNA replication

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A single ataxia telangiectasia gene with a product similar to PI-3 kinase

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The DNA double-strand break repair gene hMRE11 is mutated in individuals with an ataxia-telangiectasia-like disorder

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The Nijmegen breakage syndrome protein is essential for Mre11 phosphorylation upon DNA damage

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Functional link between ataxia-telangiectasia and Nijmegen breakage syndrome gene products

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Cell cycle checkpoint signaling through the ATM and ATR kinases

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Onset of catalytic activity of gold clusters on titania with the appearance of nonmetallic properties

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ATM associates with and phosphorylates p53: mapping the region of interaction

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

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Ataxia telangiectasia-mutated phosphorylates Chk2 in vivo and in vitro

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A mammalian cell cycle checkpoint pathway utilizing p53 and GADD45 is defective in ataxia-telangiectasia

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Chk2 activation dependence on Nbs1 after DNA damage

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Involvement of Brca1 in S-phase and G(2)-phase checkpoints after ionizing irradiation

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Isolation of full-length ATM cDNA and correction of the ataxia-telangiectasia cellular phenotype

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Oligomeric ring structure of the Bloom's syndrome helicase

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The genetic defect in ataxia-telangiectasia

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

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

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ATM phosphorylation of Nijmegen breakage syndrome protein is required in a DNA damage response

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ATM--a key determinant of multiple cellular responses to irradiation

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ATM-dependent phosphorylation and accumulation of endogenous BLM protein in response to ionizing radiation

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Regulation and localization of the Bloom syndrome protein in response to DNA damage

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Potential role for the BLM helicase in recombinational repair via a conserved interaction with RAD51

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Bloom's syndrome protein is required for correct relocalization of RAD50/MRE11/NBS1 complex after replication fork arrest

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Radiation sensitivity of Bloom's syndrome lymphocytes during S and G2 phases

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

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Identifiers

DOI

10.1074/JBC.M203801200

1 reference

Consolidated OpenCitations Corpus – April 2017

3417827

3417827

1 reference

Consolidated OpenCitations Corpus – April 2017

Consolidated OpenCitations Corpus – April 2017

1 reference