Histone H2AX: a dosage-dependent suppressor of oncogenic translocations and tumors (Q64387467)

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6 November 2019

title

Histone H2AX: a dosage-dependent suppressor of oncogenic translocations and tumors (English)

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6 November 2019

author name string

Craig H Bassing

1

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6 November 2019

Heikyung Suh

2

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6 November 2019

David O Ferguson

3

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6 November 2019

Katrin F Chua

4

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6 November 2019

John Manis

5

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6 November 2019

Mark Eckersdorff

6

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6 November 2019

Megan Gleason

7

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6 November 2019

Rodrick Bronson

8

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6 November 2019

Charles Lee

9

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6 November 2019

Frederick W Alt

10

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6 November 2019

language of work or name

English

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publication date

1 August 2003

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6 November 2019

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6 November 2019

volume

114

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6 November 2019

page(s)

359-370

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6 November 2019

issue

3

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Positive selection of thymocytes: the long and winding road.

6 November 2019

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ATM phosphorylates histone H2AX in response to DNA double-strand breaks

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ATR Regulates Fragile Site Stability

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H2AX haploinsufficiency modifies genomic stability and tumor susceptibility

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Response to RAG-mediated VDJ cleavage by NBS1 and gamma-H2AX

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A class switch control region at the 3′ end of the immunoglobulin heavy chain locus

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Evidence for replicative repair of DNA double-strand breaks leading to oncogenic translocation and gene amplification

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Mice deficient for p53 are developmentally normal but susceptible to spontaneous tumours

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A role for Saccharomyces cerevisiae histone H2A in DNA repair.

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DNA damage-induced G2-M checkpoint activation by histone H2AX and 53BP1

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H2AX is required for chromatin remodeling and inactivation of sex chromosomes in male mouse meiosis

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7 January 2021

Cancer biology. A matter of dosage

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Phosphorylation of histone H2AX and activation of Mre11, Rad50, and Nbs1 in response to replication-dependent DNA double-strand breaks induced by mammalian DNA topoisomerase I cleavage complexes.

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The RAG-1/2 endonuclease causes genomic instability and controls CNS complications of lymphoblastic leukemia in p53/Prkdc-deficient mice.

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MDC1 is required for the intra-S-phase DNA damage checkpoint

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Chk2 is a tumor suppressor that regulates apoptosis in both an ataxia telangiectasia mutated (ATM)-dependent and an ATM-independent manner

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Chk2 is dispensable for p53-mediated G1 arrest but is required for a latent p53-mediated apoptotic response

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7 January 2021

Tumor spectrum analysis in p53-mutant mice

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7 January 2021

Sensing and repairing DNA double-strand breaks

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7 January 2021

Mutation and cancer: statistical study of retinoblastoma

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No requirement for V(D)J recombination in p53-deficient thymic lymphoma

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7 January 2021

MDC1 is coupled to activated CHK2 in mammalian DNA damage response pathways

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7 January 2021

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7 January 2021

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Identifiers

DOI

1 reference

https://www.ebi.ac.uk/europepmc/webservices/rest/search?query=EXT_ID:12914700%20AND%20SRC:MED&resulttype=core&format=json

6 November 2019

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