Publication Date:
2008-05-10
Description:
As obligate intracellular parasites, viruses expertly modify cellular processes to facilitate their replication and spread, often by encoding genes that mimic the functions of cellular proteins while lacking regulatory features that modify their activity. We show that the human cytomegalovirus UL97 protein has activities similar to cellular cyclin-cyclin-dependent kinase (CDK) complexes. UL97 phosphorylated and inactivated the retinoblastoma tumor suppressor, stimulated cell cycle progression in mammalian cells, and rescued proliferation of Saccharomyces cerevisiae lacking CDK activity. UL97 is not inhibited by the CDK inhibitor p21 and lacks amino acid residues conserved in the CDKs that permit the attenuation of kinase activity. Thus, UL97 represents a functional ortholog of cellular CDKs that is immune from normal CDK control mechanisms.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hume, Adam J -- Finkel, Jonathan S -- Kamil, Jeremy P -- Coen, Donald M -- Culbertson, Michael R -- Kalejta, Robert F -- AI26077/AI/NIAID NIH HHS/ -- GM65172/GM/NIGMS NIH HHS/ -- R56-AI064703/AI/NIAID NIH HHS/ -- T32 AI07245/AI/NIAID NIH HHS/ -- T32 CA009135-31/CA/NCI NIH HHS/ -- T32 GM007215/GM/NIGMS NIH HHS/ -- T32 GM077078-01/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2008 May 9;320(5877):797-9. doi: 10.1126/science.1152095.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute for Molecular Virology and McArdle Laboratory for Cancer Research, University of Wisconsin-Madison, Madison, WI 53706, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18467589" target="_blank"〉PubMed〈/a〉
Keywords:
Cell Cycle
;
Cell Line
;
Cyclin-Dependent Kinases/antagonists & inhibitors/*metabolism
;
Cytomegalovirus/enzymology/*physiology
;
Humans
;
Molecular Mimicry
;
Phosphorylation
;
Phosphotransferases (Alcohol Group Acceptor)/antagonists & inhibitors/*metabolism
;
Protein Kinase Inhibitors/pharmacology
;
Retinoblastoma Protein/*metabolism
Print ISSN:
0036-8075
Electronic ISSN:
1095-9203
Topics:
Biology
,
Chemistry and Pharmacology
,
Computer Science
,
Medicine
,
Natural Sciences in General
,
Physics
Permalink
