scholarly journals Genetic analysis of hyperemesis gravidarum reveals association with intracellular calcium release channel (RYR2)

2017 ◽  
Vol 439 ◽  
pp. 308-316 ◽  
Author(s):  
Marlena Schoenberg Fejzo ◽  
Ronny Myhre ◽  
Lucía Colodro-Conde ◽  
Kimber W. MacGibbon ◽  
Janet S. Sinsheimer ◽  
...  
Keyword(s):  
Genetic Analysis ◽  
Intracellular Calcium ◽  
Calcium Release ◽  
Hyperemesis Gravidarum ◽  
Calcium Release Channel ◽  
Release Channel ◽  
Intracellular Calcium Release

Polycystin-2 is an intracellular calcium release channel

2002 ◽  
Vol 4 (3) ◽  
pp. 191-197 ◽  
Author(s):  
Peter Koulen ◽  
Yiqiang Cai ◽  
Lin Geng ◽  
Yoshiko Maeda ◽  
Sayoko Nishimura ◽  
...  
Keyword(s):  
Intracellular Calcium ◽  
Calcium Release ◽  
Calcium Release Channel ◽  
Release Channel ◽  
Intracellular Calcium Release

scholarly journals T cells deficient in inositol 1,4,5-trisphosphate receptor are resistant to apoptosis.

1997 ◽  
Vol 17 (6) ◽  
pp. 3005-3012 ◽  
Author(s):  
T Jayaraman ◽  
A R Marks
Keyword(s):  
T Cells ◽  
Intracellular Calcium ◽  
Calcium Release ◽  
Calcium Influx ◽  
Cell Receptor ◽  
Calcium Release Channel ◽  
Release Channel ◽  
Inositol 1,4,5 Trisphosphate ◽  
Intracellular Calcium Release ◽  
Trisphosphate Receptor

The type 1 inositol 1,4,5-trisphosphate receptor (IP3R1) calcium release channel is present on the endoplasmic reticulum of most cell types. T lymphocytes which have been made deficient in IP3R1 lack detectable IP3-induced intracellular calcium release and exhibit defective signaling via the T-cell receptor (TCR) (T. Jayaraman, E. Ondriasova, K. Ondrias, D. Harnick, and A. R. Marks, Proc. Natl. Acad. Sci. USA 92:6007-6011, 1995). We now show that IP3R1-deficient T cells are resistant to apoptosis induced by dexamethasone, TCR stimulation, ionizing radiation, and Fas. Resistance to TCR-mediated apoptosis in IP3R1-deficient cells is reversed by pharmacologically raising cytoplasmic calcium levels. TCR-mediated apoptosis can be induced in calcium-free media, indicating that extracellular calcium influx is not required. These findings suggest that intracellular calcium release via the IP3R1 is a critical mediator of apoptosis.

scholarly journals Intracellular Calcium Release Channel Expression during Embryogenesis

1999 ◽  
Vol 206 (2) ◽  
pp. 163-177 ◽  
Author(s):  
Nora Rosemblit ◽  
Maria C. Moschella ◽  
Elena Ondria s̆ ◽  
David E. Gutstein ◽  
Karol Ondria s̆ ◽  
...  
Keyword(s):  
Intracellular Calcium ◽  
Calcium Release ◽  
Calcium Release Channel ◽  
Release Channel ◽  
Channel Expression ◽  
Intracellular Calcium Release

Carnosine is a novel peptide modulator of intracellular calcium and contractility in cardiac cells

1997 ◽  
Vol 272 (1) ◽  
pp. H462-H468 ◽  
Author(s):  
G. P. Zaloga ◽  
P. R. Roberts ◽  
K. W. Black ◽  
M. Lin ◽  
G. Zapata-Sudo ◽  
...  
Keyword(s):  
Intracellular Calcium ◽  
Lipid Bilayers ◽  
Ryanodine Receptor ◽  
Calcium Release ◽  
Cardiac Contractility ◽  
Cardiac Cells ◽  
Dependent Manner ◽  
Calcium Release Channel ◽  
Release Channel ◽  
Contractile Failure

Myocardial contractile failure is a common cause of morbidity and mortality in patients with ischemic heart disease and systemic inflammatory states such as sepsis. Accumulating evidence indicates that contractile failure is associated with dysregulation of myoplasmic calcium levels. In a search for biochemical causes for contractile dysfunction, we found that the dipeptide carnosine improves cardiac contractility and tested the possibility that carnosine plays a role in the regulation of intracellular calcium. Carnosine increased contractility in a dose-dependent manner (1-10 mM) in isolated perfused rat hearts. and it also increased free intracellular calcium levels in isolated myocytes. Carnosine increased myocyte tension via calcium release from the ryanodine receptor calcium release channel in skinned myocardial fibers and increased open-state probability and dwell time of the isolated ryanodine receptor calcium release channel in lipid bilayers. In addition. we report that carnosine sensitizes the contractile proteins so calcium. These results suggest a novel role for carnosine as a modulator of intracellular calcium and contractility in cardiac tissue.

Ceramide triggers intracellular calcium release via the IP3 receptor inXenopus laevisoocytes

1999 ◽  
Vol 277 (4) ◽  
pp. C665-C672 ◽  
Author(s):  
Evgeny Kobrinsky ◽  
Andrew I. Spielman ◽  
Sophia Rosenzweig ◽  
Andrew R. Marks
Keyword(s):  
Intracellular Calcium ◽  
Signaling Pathways ◽  
Calcium Release ◽  
Second Messenger ◽  
Xenopus Laevis Oocytes ◽  
Calcium Stores ◽  
Ip3 Receptor ◽  
Calcium Release Channel ◽  
Release Channel ◽  
Phosphoinositide Signaling

Ceramide, a product of sphingomyelin turnover, is a lipid second messenger that mediates diverse signaling pathways, including those leading to cell cycle arrest and differentiation. The mechanism(s) by which ceramide signals downstream events have not been fully elucidated. Here we show that, in Xenopus laevis oocytes, ceramide-induced maturation is associated with the release of intracellular calcium stores. Ceramide caused a dose-dependent elevation in the second messenger inositol 1,4,5-trisphosphate (IP3) via activation of Gq/11α and phospholipase C-βX. Elevation of IP3, in turn, activated the IP3 receptor calcium release channel on the endoplasmic reticulum, resulting in a rise in cytoplasmic calcium. Thus our study demonstrates that cross talk between the ceramide and phosphoinositide signaling pathways modulates intracellular calcium homeostasis.

scholarly journals “Ryanopathies” and RyR2 dysfunctions: can we further decipher them using in vitro human disease models?

2021 ◽  
Vol 12 (11) ◽  
Author(s):  
Yvonne Sleiman ◽  
Alain Lacampagne ◽  
Albano C. Meli
Keyword(s):  
Intracellular Calcium ◽  
Ryanodine Receptor ◽  
Calcium Release ◽  
Current Knowledge ◽  
Cell Types ◽  
Calcium Release Channel ◽  
Release Channel ◽  
Cellular Environment ◽  
Intracellular Ca

AbstractThe regulation of intracellular calcium (Ca2+) homeostasis is fundamental to maintain normal functions in many cell types. The ryanodine receptor (RyR), the largest intracellular calcium release channel located on the sarco/endoplasmic reticulum (SR/ER), plays a key role in the intracellular Ca2+ handling. Abnormal type 2 ryanodine receptor (RyR2) function, associated to mutations (ryanopathies) or pathological remodeling, has been reported, not only in cardiac diseases, but also in neuronal and pancreatic disorders. While animal models and in vitro studies provided valuable contributions to our knowledge on RyR2 dysfunctions, the human cell models derived from patients’ cells offer new hope for improving our understanding of human clinical diseases and enrich the development of great medical advances. We here discuss the current knowledge on RyR2 dysfunctions associated with mutations and post-translational remodeling. We then reviewed the novel human cellular technologies allowing the correlation of patient’s genome with their cellular environment and providing approaches for personalized RyR-targeted therapeutics.

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