Inositol phosphates and Ca2+ entry: toward a proliferation or a simplification?
Intracellular mobilization of Ca2+ by inositol trisphosphate (IP3) is only a temporary phenomenon; the more crucial process of stimulated entry of Ca2+ by inositol phosphates is still poorly understood, with apparently conflicting data and hypotheses arising from different tissues and experimental protocols. There is clear evidence that the intracellular Ca2+ stores themselves can control Ca2+ entry and that IP3 may exert a direct effect on Ca2+ entry over and above its function in emptying those stores. There is also clear evidence that inositol tetrakisphosphate (IP4) can control Ca2+ entry, but there is controversy over whether it is actually necessary. Thus at present the combined evidence suggests that there must be a multiplicity of mechanisms extant, with different mechanisms being emphasized in different tissues. Alternatively, there could be one common mechanism, discussed here, which may lead to apparently different emphases as a result of the various experimental protocols.
Irvine
R F
RF
Department of Biochemistry, AFRC Institute of Animal Physiology and Genetics Research, Babraham, Cambridge, U.K.
D000818:Animals; D001692:Biological Transport; D002118:Calcium / Q000378:metabolism*; D002462:Cell Membrane / Q000378:metabolism; D004721:Endoplasmic Reticulum / Q000378:metabolism; D006801:Humans; D007295:Inositol Phosphates / Q000378:metabolism*; D011956:Receptors, Cell Surface / Q000378:metabolism
D007295:Inositol Phosphates; D011956:Receptors, Cell Surface; D002118:Calcium