Linked Life Data

17555746

Source:http://linkedlifedata.com/resource/pubmed/id/17555746

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
19
pubmed:dateCreated
2007-7-27
pubmed:abstractText
Many types of cancer cells constitutively express major molecular chaperones at high levels. Recent findings demonstrate that specific depletion of individual chaperones, including various members of the Hsp70 family, small heat shock proteins, or VCP/p97, leads to activation of p53 pathway and subsequently triggers cellular senescence. Here, we discuss a possibility that in cancer cells high levels of chaperones serve to keep the p53 signaling under control, thus allowing cancer cells to evade the default senescence and form tumors.
pubmed:commentsCorrections
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jul
pubmed:issn
0014-5793
pubmed:author
pubmed:issnType
Print
pubmed:day
31
pubmed:volume
581
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
3711-5
pubmed:dateRevised
2008-1-28
pubmed:meshHeading
pubmed:year
2007
pubmed:articleTitle
Molecular chaperones regulate p53 and suppress senescence programs.
pubmed:affiliation
Department of Biochemistry, Boston University Medical School, 715 Albany Street, K323, Boston, MA 02118, United States. sherma1@bu.edu
pubmed:publicationType
Journal Article, Review