Linked Life Data

14499348

Source:http://linkedlifedata.com/resource/pubmed/id/14499348

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
11
pubmed:dateCreated
2003-9-22
pubmed:abstractText
Calcium is a second messenger that is implicated in the regulation of cell cycle transitions. Calmodulin is a ubiquitous protein that translates intracellular calcium signals and activates several enzymes including calcium/calmodulin-dependent protein kinase II (CaMKII). Pharmacological inhibitors and constitutively active mutants have implicated CaMKII in cell cycle mediation. Specifically, constitutively active CaMKII impedes mitosis. In order to elucidate the molecular mechanisms underlying this phenomenon, the effect of constitutively active CaMKII gene expression on cdc2/cyclin B1 was investigated. As seen in previous studies with S. pombe, constitutively active CaMKII-hindered mitosis. However, this report shows that CaMKII does not cause permanent cell cycle arrest but delays progression into mitosis. Constitutive CaMKII expression also leads to elevations in cyclin B1 expression and cdc2 tyrosine-15 phosphorylation, analogous to observations in cells treated with hydroxyurea. Taken together, these data suggest that constitutive CaMKII may delay mitosis by activating a cell cycle checkpoint.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Nov
pubmed:issn
0898-6568
pubmed:author
pubmed:issnType
Print
pubmed:volume
15
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1049-57
pubmed:dateRevised
2009-11-19
pubmed:meshHeading
pubmed:year
2003
pubmed:articleTitle
CyclinB1 expression is elevated and mitosis is delayed in HeLa cells expressing autonomous CaMKII.
pubmed:affiliation
Department of Molecular and Cellular Physiology, University of Cincinnati College of Medicine, Cincinnati, OH 45267, USA.
pubmed:publicationType
Journal Article