Linked Life Data

17227549

Source:http://linkedlifedata.com/resource/pubmed/id/17227549

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
6
pubmed:dateCreated
2007-1-17
pubmed:abstractText
The ATR and ATM protein kinases are known to be involved in a wide variety of responses to DNA damage. The Arabidopsis thaliana genome includes both ATR and ATM orthologs, and plants with null alleles of these genes are viable. Arabidopsis atr and atm mutants display hypersensitivity to gamma-irradiation. To further characterize the roles of ATM and ATR in response to ionizing radiation, we performed a short-term global transcription analysis in wild-type and mutant lines. We found that hundreds of genes are upregulated in response to gamma-irradiation, and that the induction of virtually all of these genes is dependent on ATM, but not ATR. The transcript of CYCB1;1 is unique among the cyclin transcripts in being rapidly and powerfully upregulated in response to ionizing radiation, while other G(2)-associated transcripts are suppressed. We found that both ATM and ATR contribute to the induction of a CYCB1;1:GUS fusion by IR, but only ATR is required for the persistence of this response. We propose that this upregulation of CYCB1;1 does not reflect the accumulation of cells in G(2), but instead reflects a still unknown role for this cyclin in DNA damage response.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Dec
pubmed:issn
0960-7412
pubmed:author
pubmed:issnType
Print
pubmed:volume
48
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
947-61
pubmed:dateRevised
2007-11-15
pubmed:meshHeading
pubmed:year
2006
pubmed:articleTitle
ATR and ATM play both distinct and additive roles in response to ionizing radiation.
pubmed:affiliation
Department of Biochemistry and Molecular Biology, University of New Hampshire, Durham, NH 03824, USA. k.culligan@unh.edu
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, Non-P.H.S., Research Support, Non-U.S. Gov't