Linked Life Data

16997458

Source:http://linkedlifedata.com/resource/pubmed/id/16997458

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
2007-3-27
pubmed:abstractText
There is much controversy in the literature regarding the role of p53 status response on hypoxia inducible factor (HIF) signaling in response to chronic relative hypoxia (CRH). The goal of this paper was to methodically examine this response in isogenically matched tumor cells. We report that p53-mutant (MUT) cells, versus p53-wild-type (WT) cells, showed decreased apoptosis, increased cell proliferation with higher basal HIF-1alpha levels in response to CRH. In addition, we found increased HIF-mediated transactivation and increased VEGF release with decreased HIF-1alpha/p53 and HIF-1alpha/MDM-2 partnering in p53-MUT versus p53-WT cells in response to CRH.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
May
pubmed:issn
0304-3835
pubmed:author
pubmed:issnType
Print
pubmed:day
8
pubmed:volume
249
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
209-19
pubmed:meshHeading
pubmed:year
2007
pubmed:articleTitle
Mutant p53 facilitates pro-angiogenic, hyperproliferative phenotype in response to chronic relative hypoxia.
pubmed:affiliation
Department of Cell Biology, University of Oklahoma Health Sciences Center, 726 BMSB, 940 S.L. Young Boulevard, Oklahoma City, OK, USA.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't