Linked Life Data

15464845

Source:http://linkedlifedata.com/resource/pubmed/id/15464845

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
2004-10-6
pubmed:abstractText
Poxvirus infection has a strong effect on cellular functions. To understand viral pathogenesis, it is necessary to know how viral proteins interact with host proteins. The B1R kinase is an early viral gene required for vaccinia virus DNA synthesis and replication, but no cellular substrate is known for this viral kinase. B1R is able to hyperphosphorylate p53 in several residues in the N-terminal transactivation domain, including Ser15 and Thr18. B1R does not phosphorylate Mdm2. B1R promotes an increase in p53 ubiquitination and a reduction of p53 acetylation by p300. The over-expressed B1R protein induces the degradation of p53 in a concentration-dependent manner and is lost when Ser15 and Th18 are changed to alanine or when the B1R kinase is inactivated by introducing the K149Q substitution. The B1R-induced downregulation of p53 requires Mdm2. The hyperphosphorylated p53 is transcriptionally active, and this activity also falls as B1R increases. The BAX gene promoter is more sensitive to this reduction of transcription than p21 or 14-3-3 gene promoters. This effect of B1R on p53 can be one of the mechanisms by which vaccinia virus exerts its role in infected cells.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Oct
pubmed:issn
0042-6822
pubmed:author
pubmed:issnType
Print
pubmed:day
25
pubmed:volume
328
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
254-65
pubmed:dateRevised
2007-11-15
pubmed:meshHeading
pubmed:year
2004
pubmed:articleTitle
The vaccinia virus B1R kinase induces p53 downregulation by an Mdm2-dependent mechanism.
pubmed:affiliation
Instituto de Biología Molecular y Celular del Cáncer, Consejo Superior de Investigaciones Científicas, Universidad de Salamanca, E-37007 Salamanca, Spain.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't