Calcium -induced channel

The NHR contains also the conserved Calcineurin docking site, PxlxIT, required for the physical interaction of NEAT and Calcineurin. Dephosphorylation of at least 13 serines residues in the NHR induces a conformational change that exposes the nuclear localization sequences (NLS), allowing the nuclear translocation of NEAT. Rephosphorylation of these residues unmasks the nuclear export sequences that direct transport back to the cytoplasm. Engagement of receptors such as the antigen receptors in T and B cells is coupled to phospholipase C activation and subsequent production of inositol triphosphate. Increased levels of inositol triphosphate lead to the initial release of intracellular stores of calcium. This early increase of calcium induces opening of the plasma membrane calcium-released-activated-calcium (CRAC) channels,... 

In addition to the well-known iron effects on peroxidative processes, there are also other mechanisms of iron-initiated free radical damage, one of them, the effect of iron ions on calcium metabolism. It has been shown that an increase in free cytosolic calcium may affect cellular redox balance. Stoyanovsky and Cederbaum [174] showed that in the presence of NADPH or ascorbic acid iron ions induced calcium release from liver microsomes. Calcium release occurred only under aerobic conditions and was inhibited by antioxidants Trolox C, glutathione, and ascorbate. It was suggested that the activation of calcium releasing channels by the redox cycling of iron ions may be an important factor in the stimulation of various hepatic disorders in humans with iron overload. 

Creed KE, Ishikawa S, Ito Y 1983 Electrical and mechanical activity recorded from rabbit urinary bladder in response to nerve stimulation. J Physiol 338 149-164 Cui J, Cox DH, Aldrich RW 1997 Intrinsic voltage dependence and Ca2+ regulation of mslo large conductance Ca-activated K+ channels. J Gen Physiol 109 647-673 Fabiato A 1983 Calcium-induced release of calcium from the cardiac sarcoplasmic reticulum. Am J Physiol 245 0-04... 

Skeletal muscle is activated by nerve impulses which induce Ca2+ release through the action of a voltage sensor, a protein also known as the dihydropyridine receptor,wx together with a calcium release channel known as the ryanodine... 

Terentyev, D., Nori, A., Santoro, M., Viatchenko-Karpinski, S., Kubalova, Z., Gyorke, I., Terentyeva, R., Vedamoorthyrao, S., Blom, N. A., Valle, G., Napolitano, C., Williams, S. C., Volpe, P., Priori, S. G., and Gyorke, S. (2006). Abnormal Interactions of Calsequestrin with the Ryanodine Receptor Calcium Release Channel Complex Linked to Exercise-Induced Sudden Cardiac Death. Circ Res 98(9) 1151-8. 

Figure 2. A proposed model demonstrating several different prominent calcium-related pathways whose activity may be altered in dystrophic muscle. Increased activity of mechanosensitive channels (MS) and store-activated channels (SOC), which are likely derived from the same gene product (TRPC), and the calcium leak channel, which could represent a proteolyzed TRPC SOC channel. Decreased mechanical coupling between L-type VGCC and ryanodine receptors may increase basal calcium release from calcium stores (not shown). Further, increased IP, and IP, receptor levels may also enhance basal and stimulated calcium-induced calcium release (CICR) from calcium stores. Calcium store depletion can increase translocation of SOCs from intracellular vesicles to the sarcolemma. Finally, the relationship between increased membrane fragility and tearing is less certain, but calcium influx through sarcolemmal tears could lead to calcium-dependent proteolysis and increased activity of calcium leak channels, as well as proteolysis of other targets, and increased release of calcium from intracellular stores through CICR. This model is not meant to be comprehensive, and other calcium-related molecules are discussed in the text...

Wehrens, X.H., Lehnart, S.E., Huang, F., et al., 2003, FKBP12.6 deficiency and defective calcium release channel (ryanodine receptor) function hnked to exercise-induced sudden cardiac death. Cell, 113(7), pp 829-40. 

Hlubek MD, Stuenkel EL, Krasnoperov VG et al (2000) Calcium-independent receptor for a-latrotoxin and neurexin la facilitate toxin-induced channel formation evidence that channel formation results from tethering of toxin to membrane. Mol Pharmacol 57 519-28 Hurlbut WP, Ceccarelli B (1979) Use of black widow spider venom to study the release of neurotransmitters. Adv Cytopharmacol 3 87-115 87-115 Hurlbut WP, Chieregatti E, Valtorta F et al (1994) a-Latrotoxin channels in neuroblastoma cells. JMembr Biol 138 91-102... 

Derived from Hodgkin-Huxley s celebrated theory and inspired by the experimental observations, cellular calcium dynamics, either stimulated via inositol 1,4,5-trisphosphate (IP3) receptor in many non-muscle cells [69,139], or via the ryanodine receptor in muscle cells [108], is another extensively studied oscillatory system. Both receptors are themselves Ca2+ channels, and both can be activated by Ca2+, leading to calcium-induced calcium release from endoplasmic reticulum. 

Rosenmund C, Westbrook GL (1993) Calcium-induced actin depolymerization reduces NMDA channel activity. Neuron 70 805-814. 

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