Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
4
pubmed:dateCreated
2010-4-19
pubmed:abstractText
Viral K-cyclin derived from Kaposi's sarcoma-associated herpesvirus is homologous with mammalian D-type cyclins. Here, we demonstrated the regulatory mechanisms for K-cyclin function and degradation in human embryonic kidney HEK293 and primary effusion lymphoma JSC-1 cell lines. Proteasome inhibitor MG132 treatment induced an accumulation of ubiquitinated K-cyclin in these cells, and co-expression of CDK6 prevented K-cyclin ubiquitination. Also K-cyclin mutants incompetent for CDK6-binding were destabilized by proteasome pathway. Furthermore, silencing of p16INK4a promoted K-cyclin-CDK6 complex formation and hence induced K-cyclin-associated kinase activity in HEK293 cells. These observations indicate that CDK6-bound K-cyclin is functionally stable but monomeric K-cyclin is targeted to ubiquitin-dependent degradation pathway in these cells. Our data suggest that the balance between CDK6 and p16INK4a regulates the availability of functional K-cyclin in human cells.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Apr
pubmed:issn
1090-2104
pubmed:author
pubmed:copyrightInfo
2010 Elsevier Inc. All rights reserved.
pubmed:issnType
Electronic
pubmed:day
16
pubmed:volume
394
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1000-5
pubmed:meshHeading
pubmed:year
2010
pubmed:articleTitle
Functional availability of gamma-herpesvirus K-cyclin is regulated by cellular CDK6 and p16INK4a.
pubmed:affiliation
Division of Chemotherapy, Faculty of Pharmacy, Keio University, 1-5-30 Shiba-koen, Minato-ku, Tokyo 105-8512, Japan.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't