Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
5
pubmed:dateCreated
2011-8-1
pubmed:abstractText
Changes in the concentration and spatial distribution of Ca(2+) ions in the cytoplasm constitute a ubiquitous intracellular signaling module in cellular physiology. With the advent of Ca(2+) dyes that allow direct visualization of Ca(2+) transients, combined with powerful experimental tools such as electrophysiological recordings, intracellular Ca(2+) transients have been implicated in practically every aspect of cellular physiology, including cellular proliferation. Ca(2+) signals are associated with different phases of the cell cycle and interfering with Ca(2+) signaling or downstream pathways often disrupts progression of the cell cycle. Although there exists a dependence between Ca(2+) signals and the cell cycle the mechanisms involved are not well defined and given the cross-talk between Ca(2+) and other signaling modules, it is difficult to assess the exact role of Ca(2+) signals in cell cycle progression. Two exceptions however, include fertilization and T-cell activation, where well-defined roles for Ca(2+) signals in mediating progression through specific stages of the cell cycle have been clearly established. In the case of T-cell activation Ca(2+) regulates entry into the cell cycle through the induction of gene transcription.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
May
pubmed:issn
1532-1991
pubmed:author
pubmed:issnType
Electronic
pubmed:volume
49
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
323-30
pubmed:meshHeading
pubmed:year
2011
pubmed:articleTitle
Ca(2+) signaling, genes and the cell cycle.
pubmed:affiliation
Department of Physiology and Biophysics, Weill Cornell Medical College in Qatar, PO Box 24144, Education City – Qatar Foundation, Doha, Qatar. Khm2002@qatar-med.cornell.edu
pubmed:publicationType
Journal Article, Review, Research Support, Non-U.S. Gov't, Research Support, N.I.H., Extramural