Abstract
Calcium (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.
Highlights
Intracellular Ca2+ can regulate cellular processes as distinct as cell death and proliferation [1]
PIP kinase (PIPK) and PIP2 are present in the interior of the nucleus [14], and insulin and hepatocyte growth factor (HGF) can induce InsP3 production in nuclei [6,7,35]
These findings suggest that Ca2+ signaling machinery is present along the nuclear envelope but within the interior of the nucleus as well, which may provide an additional level of spatial control of nuclear Ca2+ signaling
Summary
Intracellular Ca2+ can regulate cellular processes as distinct as cell death and proliferation [1]. Ca2+ can spread passively from the cytosol into the nucleus under certain circumstances [25,26,27], intranuclear InsP3 can increase Ca2+ directly within the nucleus as well, both in isolated nuclei [12,20,28] and in nuclei within intact cells [23,29,30]. The relative distribution of InsP3R isoforms in the nucleus and cytosol can differ among cell types [21].
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