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The FASEB Journal, Vol 6, 3085-3091, Copyright © 1992 by The Federation of American Societies for Experimental Biology
REVIEWS |
RF Irvine
Department of Biochemistry, AFRC Institute of Animal Physiology and Genetics Research, Babraham, Cambridge, U.K.
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.
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