Linked Life Data

1570154

Source:http://linkedlifedata.com/resource/pubmed/id/1570154

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
5
pubmed:dateCreated
1992-5-28
pubmed:abstractText
The ability of the oncogene products of DNA tumor viruses to induce DNA synthesis in quiescent cells is thought to depend on their capacity to bind to cellular proteins such as the retinoblastoma-suppressor protein Rb and the tumor suppressor p53, thereby abolishing the growth-arresting properties of these proteins. We have tested this hypothesis using SV40 T antigens carrying lesions that affect Rb binding, p53 binding or other functions involved in cell transformation. The results demonstrate that Rb binding is not essential for growth stimulation by T antigen. However, detailed analysis, including intracistronic complementation, suggests that at least three functions, Rb binding, a novel second activity localized to the DNA-binding domain and a function residing in the carboxy terminus, probably p53 binding, cooperate to generate the full growth induction potential of T antigen.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
May
pubmed:issn
0950-9232
pubmed:author
pubmed:issnType
Print
pubmed:volume
7
pubmed:geneSymbol
Rb, p53
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
837-47
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed:year
1992
pubmed:articleTitle
Intracistronic complementation reveals a new function of SV40 T antigen that co-operates with Rb and p53 binding to stimulate DNA synthesis in quiescent cells.
pubmed:affiliation
Institute for Biochemistry, Munich, Germany.
pubmed:publicationType
Journal Article, In Vitro, Research Support, Non-U.S. Gov't