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pubmed-article:18982194pubmed:dateCreated2009-2-16lld:pubmed
pubmed-article:18982194pubmed:abstractTextCalcium (Ca2+) is a versatile second messenger that regulates a wide range of cellular functions. Although it is not established how a single second messenger coordinates diverse effects within a cell, there is increasing evidence that the spatial patterns of Ca2+ signals may determine their specificity. Ca2+ signaling patterns can vary in different regions of the cell and Ca2+ signals in nuclear and cytoplasmic compartments have been reported to occur independently. No general paradigm has been established yet to explain whether, how, or when Ca2+ signals are initiated within the nucleus or their function. Here we highlight that receptor tyrosine kinases rapidly translocate to the nucleus. Ca2+ signals that are induced by growth factors result from phosphatidylinositol 4,5-bisphosphate hydrolysis and inositol 1,4,5-trisphosphate formation within the nucleus rather than within the cytoplasm. This novel signaling mechanism may be responsible for growth factor effects on cell proliferation.lld:pubmed
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pubmed-article:18982194pubmed:authorpubmed-author:RodriguesM...lld:pubmed
pubmed-article:18982194pubmed:authorpubmed-author:NathansonM...lld:pubmed
pubmed-article:18982194pubmed:authorpubmed-author:GomesD ADAlld:pubmed
pubmed-article:18982194pubmed:authorpubmed-author:LeiteM FMFlld:pubmed
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pubmed-article:18982194pubmed:volume42lld:pubmed
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pubmed-article:18982194pubmed:pagination17-20lld:pubmed
pubmed-article:18982194pubmed:dateRevised2011-3-8lld:pubmed
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pubmed-article:18982194pubmed:year2009lld:pubmed
pubmed-article:18982194pubmed:articleTitleNuclear calcium signaling: a cell within a cell.lld:pubmed
pubmed-article:18982194pubmed:affiliationDepartamento de Fisiologia e Biofísica, Universidade Federal de Minas Gerais, Belo Horizonte, MG, Brasil.lld:pubmed
pubmed-article:18982194pubmed:publicationTypeJournal Articlelld:pubmed
pubmed-article:18982194pubmed:publicationTypeReviewlld:pubmed
pubmed-article:18982194pubmed:publicationTypeResearch Support, Non-U.S. Gov'tlld:pubmed
pubmed-article:18982194pubmed:publicationTypeResearch Support, N.I.H., Extramurallld:pubmed
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