Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
5
pubmed:dateCreated
2007-12-12
pubmed:abstractText
The in vivo function of proteins which regulate activity of the GTPase Rac is largely unknown. Here we establish that mice lacking bcr, a known GTPase activating protein for Rac, exhibit a defect in the regulation of both hormonal and behavioral stress responses. Bcr null mutants demonstrate prolonged elevation of plasma glucocorticoids and increased fighting in males in response to physiological and social stress, respectively. Combined biochemical and behavioral data indicate that bcr is involved in mediating the cellular effects of glucocorticoids, specifically down-regulation of the stress-activated hippocampal hypothalamic-pituitary-adrenal axis.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Nov
pubmed:issn
1107-3756
pubmed:author
pubmed:issnType
Print
pubmed:volume
2
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
577-83
pubmed:dateRevised
2008-11-21
pubmed:meshHeading
pubmed:year
1998
pubmed:articleTitle
Abnormal stress response and increased fighting behavior in mice lacking the bcr gene product.
pubmed:affiliation
Division of Hematology/Oncology, Childrens Hospital of Los Angeles Research Institute, University of Southern California, 90027, USA.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't, Research Support, N.I.H., Extramural