Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
1990-5-4
pubmed:abstractText
We investigated cell cycle-dependent regulation of protein kinase activity encoded by the viral mos gene by using a normal rat kidney cell line (NRK-6m2) chronically infected with a temperature-sensitive mutant (ts110) of Moloney murine sarcoma virus, which produces the P85gag-mos transforming protein. In elutriation experiments, in which cells in various phases of the cell cycle are separated based upon size, a twofold increase in the specific activity of the P85gag-mos protein kinase was observed as cells progressed from G0/G1 through S and G2/M. A three- to fourfold increase in gas-mos protein kinase specific activity relative to unsynchronized cells was observed in mitotic NRK-6m2 cells synchronized by treatment with thymidine followed by colcemid or with nocodazole alone. Interestingly, the gag-mos protein was structurally altered in mitotic cells generating a protein species moving slower than P85gag-mos in SDS-polyacrylamide gels. Our findings indicate that viral mos protein kinase activity is regulated during the cell cycle via phosphorylation. We propose that the mos transforming protein functions in a pleiotropic manner, affecting both cytoplasmic and nuclear targets.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Feb
pubmed:issn
0950-9232
pubmed:author
pubmed:issnType
Print
pubmed:volume
5
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
171-8
pubmed:dateRevised
2009-11-19
pubmed:meshHeading
pubmed:year
1990
pubmed:articleTitle
Cell cycle-mediated structural and functional alteration of P85gag-mos protein kinase activity.
pubmed:affiliation
Department of Molecular Pathology, University of Texas M.D. Anderson Cancer Center, Houston 77030.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't