scholarly journals PML Regulates Apoptosis at Endoplasmic Reticulum by Modulating Calcium Release

Science ◽  
2010 ◽  
Vol 330 (6008) ◽  
pp. 1247-1251 ◽  
Author(s):  
C. Giorgi ◽  
K. Ito ◽  
H.-K. Lin ◽  
C. Santangelo ◽  
M. R. Wieckowski ◽  
...  
Keyword(s):  
Endoplasmic Reticulum ◽  
Calcium Release

scholarly journals Off-target effect of the cPLA2α inhibitor pyrrophenone: Inhibition of calcium release from the endoplasmic reticulum

2016 ◽  
Vol 479 (1) ◽  
pp. 61-66 ◽  
Author(s):  
Bogeon Yun ◽  
HeeJung Lee ◽  
Heather Ewing ◽  
Michael H. Gelb ◽  
Christina C. Leslie
Keyword(s):  
Endoplasmic Reticulum ◽  
Calcium Release ◽  
Target Effect

cADP-ribose releases Ca2+ from cardiac sarcoplasmic reticulum independently of ryanodine receptor

1997 ◽  
Vol 273 (3) ◽  
pp. H1082-H1089 ◽  
Author(s):  
P. Lahouratate ◽  
J. Guibert ◽  
J. F. Faivre
Keyword(s):  
Endoplasmic Reticulum ◽  
Sarcoplasmic Reticulum ◽  
Ryanodine Receptor ◽  
Sea Urchin ◽  
Calcium Release ◽  
Dependent Manner ◽  
Concentration Dependent Manner ◽  
Cardiac Sarcoplasmic Reticulum ◽  
Consistent Effect ◽  
Cyclic Adp Ribose

Cyclic ADP-ribose (cADPR), an endogenous metabolite of beta-NAD+, activates Ca2+ release from endoplasmic reticulum in sea urchin eggs via the ryanodine receptor (RyR) pathway. A similar role has been proposed in cardiac sarcoplasmic reticulum (SR), although this remains controversial. We therefore investigated the ability of cADPR to induce Ca2+ release from canine cardiac SR microsomes using fluo 3 to monitor extravesicular Ca2+ concentration. We found that cADPR induced Ca2+ release in a concentration-dependent manner, whereas neither its precursor, NAD+, nor its metabolite, ADP-ribose, elicited a consistent effect. In addition, an additive effect on calcium release between cADPR and 9-Me-7-Br-eudistomin-D (MBED), an activator of RyR, was found as well as no cross-desensitization between cADPR and MBED. Specific blockers of the RyR did not abolish the cADPR-induced Ca2+ release. These results provide evidence for cADPR-induced Ca2+ release from dog cardiac SR via a novel mechanism which is independent of RyR activation.

Heterologous expression of polycystin-1 inhibits endoplasmic reticulum calcium leak in stably transfected MDCK cells

2008 ◽  
Vol 294 (6) ◽  
pp. F1279-F1286 ◽  
Author(s):  
Kimberly H. Weber ◽  
Eun Kyung Lee ◽  
Uma Basavanna ◽  
Sabina Lindley ◽  
Roy C. Ziegelstein ◽  
...  
Keyword(s):  
Endoplasmic Reticulum ◽  
Calcium Release ◽  
Mdck Cells ◽  
Calcium Ionophore ◽  
Calcium Flux ◽  
Calcium Stores ◽  
Endoplasmic Reticulum Calcium ◽  
Calcium Indicator ◽  
Luminal Calcium ◽  
Er Membrane

We previously found that polycystin-1 accelerated the decay of ligand-activated cytoplasmic calcium transients through enhanced reuptake of calcium into the endoplasmic reticulum (ER; Hooper KM, Boletta A, Germino GG, Hu Q, Ziegelstein RC, Sutters M. Am J Physiol Renal Physiol 289: F521–F530, 2005). Calcium flux across the ER membrane is determined by the balance of active uptake and passive leak. In the present study, we show that polycystin-1 inhibited calcium leak across the ER membrane, an effect that would explain the capacity of this protein to accelerate clearance of calcium from the cytoplasm following a calcium release response. Calcium leak was detected by measurement of the accumulation of calcium in the cytoplasm following treatment with thapsigargin. Heterologous polycystin-1, stably expressed in Madin-Darby canine kidney cells, attenuated the thapsigargin-induced calcium peak with no effect on basal calcium stores, mitochondrial calcium uptake, or extrusion of calcium across the plasma membrane. The capacity of polycystin-1 to limit the rate of decay of ER luminal calcium following inhibition of the pump was shown indirectly using the calcium ionophore ionomycin, and directly by loading the ER with a low-affinity calcium indicator. We conclude that disruption of ER luminal calcium homeostasis may contribute to the cyst phenotype in autosomal dominant polycystic kidney disease.

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