Linked Life Data

15684609

Source:http://linkedlifedata.com/resource/pubmed/id/15684609

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
3
pubmed:dateCreated
2005-5-6
pubmed:databankReference
pubmed:abstractText
Ataxia telangiectasia mutated protein (ATM) is a damage response kinase that initiates a signal transduction response to the presence of DNA double strand breaks (DSBs) regulating cell cycle checkpoint arrest and apoptosis. Indirect evidence has argued that A-T cells also harbour a repair defect since unrepaired DSBs can be observed in non-replicating A-T cells after ionising radiation (IR). The basis underlying such a repair defect has remained unexplained, however. Artemis, a nuclease, whose activity is modified by phosphorylation in vitro, was recently identified as a novel ATM substrate. Artemis and ATM function in a common pathway required for the processing of a subset of double stranded DNA ends induced by IR prior to rejoining by non-homologous end-joining (NHEJ). This subset of DSBs are those normally rejoined with slow kinetics. Additional components of the ATM signal transduction pathway, Nbs1, Mre11, H2AX and 53BP1, are also required for this component of DSB repair. This process substantially contributes to survival post irradiation. Our findings add a new dimension to the ATM signal transduction response demonstrating ATM-dependent regulation of an end-processing mechanism that functions during the cell cycle delay effected by ATM.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Mar
pubmed:issn
1551-4005
pubmed:author
pubmed:issnType
Electronic
pubmed:volume
4
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
359-62
pubmed:dateRevised
2011-11-2
pubmed:meshHeading
pubmed:year
2005
pubmed:articleTitle
Artemis links ATM to double strand break rejoining.
pubmed:affiliation
Genome Damage and Stability Centre, University of Sussex, East Sussex, UK. p.a.jeggo@sussex.ac.uk
pubmed:publicationType
Journal Article, Review, Research Support, Non-U.S. Gov't