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. 1997 May 5;137(3):633–648. doi: 10.1083/jcb.137.3.633

Figure 10.

Figure 10

A hypothesis for mitochondrial modulation of capacitative Ca2+ entry. (A) When Ca2+ uptake by mitochondria is blocked, Ca2+ accumulates near CRAC channels and inhibits them (bold dashed line). A steady-state [Ca2+]i near the channels is reached as a result of this negative feedback. (B) Sequestration of Ca2+ by mitochondria in the absence of export reduces the local [Ca2+]i, thereby partially relieving inactivation of ICRAC (thin dashed line). At steady state, ICRAC is larger than in A, but much of the Ca2+ from this increased influx is sequestered and hence is not available to enhance global [Ca2+]i. (C) In the presence of normal mitochondrial uptake and release of Ca2+, mitochondria redistribute the Ca2+ derived from enhanced ICRAC to distant sites where it can elevate global [Ca2+]i.