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Store-operated Ca2+ entry: dynamic interplay between endoplasmic reticulum, mitochondria and plasma membrane
1Department of Physiology, University of Oxford, Parks Road, Oxford OX1 3PT, UK. anant.parekh@physiol.ox.ac.uk
The Journal of Physiology
|February 11, 2003
Summary
Mitochondria are essential for activating calcium release-activated calcium current (ICRAC) in eukaryotic cells. They regulate calcium influx, influencing cellular processes like exocytosis and proliferation.
Area of Science:
- Cell Biology
- Biochemistry
- Physiology
Background:
- Hormones and neurotransmitters trigger a biphasic increase in intracellular calcium, involving release from stores and subsequent influx.
- Store-operated calcium entry, particularly the calcium release-activated calcium current (ICRAC), is crucial for many cellular functions.
- The mechanism by which store depletion activates CRAC channels remains incompletely understood.
Discussion:
- This review explores experiments investigating why inositol trisphosphate (InsP3) is ineffective in activating ICRAC under physiological weak buffering conditions.
- Evidence suggests that respiring mitochondria are essential for ICRAC activation in weak intracellular calcium buffer.
- Mitochondrial calcium uptake broadens the dynamic range of InsP3 signaling for calcium influx control.
Key Insights:
- Mitochondria are critical for the activation of ICRAC under physiological conditions.
- Mitochondria regulate the extent and duration of store-operated calcium influx.
- Mitochondrial calcium buffering influences the Ca2+-dependent slow inactivation of calcium influx.
Outlook:
- Mitochondria play a vital role in all phases of store-operated calcium influx.
- Store-operated calcium entry involves a dynamic interplay between the endoplasmic reticulum, mitochondria, and plasma membrane.
- Further research into mitochondrial roles in calcium signaling could reveal new therapeutic targets.