Linked Life Data

7950913

Source:http://linkedlifedata.com/resource/pubmed/id/7950913

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
3-4
pubmed:dateCreated
1994-12-29
pubmed:abstractText
Frequent point mutations of the p53 tumor suppressor gene have been detected in solid tumors but not in acute myelogenous leukemia (AML). The inactivation of the suppressor function of the p53 protein in AML cells may be achieved through the acquisition of a mutant-like conformation. We provide evidence in this report that the p53 protein in AML cells switches to a mutant-like conformation in response to growth factor stimulation, and we propose that the conformation of p53 protein is one of the molecular mechanisms in determining whether the cells proliferate or enter apoptosis. We also show that wild-type p53 with mutant-like conformation is not equivalent to mutant p53 in their stability, which is consistent with the fact they have very different biological activities in the cells.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jul
pubmed:issn
1042-8194
pubmed:author
pubmed:issnType
Print
pubmed:volume
14
pubmed:geneSymbol
p53
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
251-5
pubmed:dateRevised
2007-11-15
pubmed:meshHeading
pubmed:year
1994
pubmed:articleTitle
Conformational change of p53 protein in growth factor-stimulated human myelogenous leukemia cells.
pubmed:affiliation
Department of Hematology, University of Texas M.D. Anderson Cancer Center, Houston 77030.
pubmed:publicationType
Journal Article, Comparative Study, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't