Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
9
pubmed:dateCreated
2003-9-15
pubmed:abstractText
Progression through the G1/S transition commits cells to synthesize DNA. Cyclin dependent kinase 2 (CDK2) is the major kinase that allows progression through G1/S phase and subsequent replication events. p27 is a CDK inhibitor (CKI) that binds to CDK2 to prevent premature activation of this kinase. Speedy (Spy1), a novel cell cycle regulatory protein, has been found to prematurely activate CDK2 when microinjected into Xenopus oocytes and when expressed in mammalian cells. To determine the mechanism underlying Spy1-induced proliferation in mammalian cell cycle regulation, we used human Spy1 as bait in a yeast two-hybrid screen to identify interacting proteins. One of the proteins isolated was p27; this novel interaction was confirmed both in vitro, using bacterially expressed and in vitro translated proteins, and in vivo, through the examination of endogenous and transfected proteins in mammalian cells. We demonstrate that Spy1 expression can overcome a p27-induced cell cycle arrest to allow for DNA synthesis and CDK2 histone H1 kinase activity. In addition, we utilized p27-null cells to demonstrate that the proliferative effect of Spy1 depends on the presence of endogenous p27. Our data suggest that Spy1 associates with p27 to promote cell cycle progression through the G1/S transition.
pubmed:grant
pubmed:commentsCorrections
http://linkedlifedata.com/resource/pubmed/commentcorrection/12972555-10075928, http://linkedlifedata.com/resource/pubmed/commentcorrection/12972555-10086358, http://linkedlifedata.com/resource/pubmed/commentcorrection/12972555-10202150, http://linkedlifedata.com/resource/pubmed/commentcorrection/12972555-10323868, http://linkedlifedata.com/resource/pubmed/commentcorrection/12972555-10375532, http://linkedlifedata.com/resource/pubmed/commentcorrection/12972555-10385618, http://linkedlifedata.com/resource/pubmed/commentcorrection/12972555-10716937, http://linkedlifedata.com/resource/pubmed/commentcorrection/12972555-11063125, http://linkedlifedata.com/resource/pubmed/commentcorrection/12972555-11352628, http://linkedlifedata.com/resource/pubmed/commentcorrection/12972555-11461916, http://linkedlifedata.com/resource/pubmed/commentcorrection/12972555-11726503, http://linkedlifedata.com/resource/pubmed/commentcorrection/12972555-11875067, http://linkedlifedata.com/resource/pubmed/commentcorrection/12972555-11980914, http://linkedlifedata.com/resource/pubmed/commentcorrection/12972555-3670292, http://linkedlifedata.com/resource/pubmed/commentcorrection/12972555-7624798, http://linkedlifedata.com/resource/pubmed/commentcorrection/12972555-7753174, http://linkedlifedata.com/resource/pubmed/commentcorrection/12972555-7859744, http://linkedlifedata.com/resource/pubmed/commentcorrection/12972555-7877684, http://linkedlifedata.com/resource/pubmed/commentcorrection/12972555-7954821, http://linkedlifedata.com/resource/pubmed/commentcorrection/12972555-8033212, http://linkedlifedata.com/resource/pubmed/commentcorrection/12972555-8033213, http://linkedlifedata.com/resource/pubmed/commentcorrection/12972555-8196612, http://linkedlifedata.com/resource/pubmed/commentcorrection/12972555-8334704, http://linkedlifedata.com/resource/pubmed/commentcorrection/12972555-8475385, http://linkedlifedata.com/resource/pubmed/commentcorrection/12972555-8524119, http://linkedlifedata.com/resource/pubmed/commentcorrection/12972555-9029151, http://linkedlifedata.com/resource/pubmed/commentcorrection/12972555-9042862, http://linkedlifedata.com/resource/pubmed/commentcorrection/12972555-9192873, http://linkedlifedata.com/resource/pubmed/commentcorrection/12972555-9311993, http://linkedlifedata.com/resource/pubmed/commentcorrection/12972555-9388487
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Sep
pubmed:issn
1059-1524
pubmed:author
pubmed:issnType
Print
pubmed:volume
14
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
3664-74
pubmed:dateRevised
2009-11-19
pubmed:meshHeading
pubmed-meshheading:12972555-3T3 Cells, pubmed-meshheading:12972555-Animals, pubmed-meshheading:12972555-CDC2-CDC28 Kinases, pubmed-meshheading:12972555-COS Cells, pubmed-meshheading:12972555-Cell Cycle Proteins, pubmed-meshheading:12972555-Cell Division, pubmed-meshheading:12972555-Cells, Cultured, pubmed-meshheading:12972555-Cercopithecus aethiops, pubmed-meshheading:12972555-Cloning, Molecular, pubmed-meshheading:12972555-Cyclin-Dependent Kinase 2, pubmed-meshheading:12972555-Cyclin-Dependent Kinase Inhibitor p27, pubmed-meshheading:12972555-Enzyme Activation, pubmed-meshheading:12972555-Enzyme Repression, pubmed-meshheading:12972555-G1 Phase, pubmed-meshheading:12972555-Mice, pubmed-meshheading:12972555-Mice, Knockout, pubmed-meshheading:12972555-Protein Binding, pubmed-meshheading:12972555-S Phase, pubmed-meshheading:12972555-Tumor Suppressor Proteins, pubmed-meshheading:12972555-Two-Hybrid System Techniques
pubmed:year
2003
pubmed:articleTitle
Spy1 interacts with p27Kip1 to allow G1/S progression.
pubmed:affiliation
Department of Chemistry and Biochemistry, University of California San Diego, La Jolla, California 92093-0367, USA.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't