The Integration of Receptor-Regulated Intracellular Calcium Release and Calcium Entry across the Plasma Membrane

1990 ◽  
pp. 111-127 ◽  
Author(s):  
JAMES W. PUTNEY
Keyword(s):  
Plasma Membrane ◽  
Intracellular Calcium ◽  
Calcium Release ◽  
Calcium Entry ◽  
Intracellular Calcium Release

scholarly journals Membrane junctions in xenopus eggs: their distribution suggests a role in calcium regulation

1983 ◽  
Vol 96 (4) ◽  
pp. 1159-1163 ◽  
Author(s):  
DM Gardiner ◽  
RD Grey
Keyword(s):  
Endoplasmic Reticulum ◽  
Plasma Membrane ◽  
Intracellular Calcium ◽  
Calcium Release ◽  
Egg Activation ◽  
Electron Dense Material ◽  
Intracellular Calcium Release ◽  
Cortical Endoplasmic Reticulum ◽  
Center Distance ◽  
Lines Of Evidence

We have observed the presence of membrane junctions formed between the plasma membrane and cortical endoplasmic reticulum of mature, unactivated eggs of xenopus laevis. The parallel, paired membranes of the junction are separated by a 10-mn gap within which electron-dense material is present. This material occurs in patches with an average center-to-center distance of approximately 30 nm. These junctions are rare in immature (but fully grown) oocytes (approximately 2 percent of the plasma membrane is associated with junctions) and increase dramatically during progesterone-induced maturation. Junctions in the mature, unactivated egg are two to three times more abundant in the animal hemisphere (25-30 percent of the plasma membrane associated with junction) as compared with the vegetal hemisphere (10-15 percent). Junction density decreases rapidly to values characteristic of immature oocytes in response to egg activation. The plasma membrane-ER junctions of xenopus eggs are strikingly similar in structure to membrane junctions in muscle cells thought to be essential in the triggering of intracellular calcium release from the sarcoplasmic reticulum. In addition, the junctions' distinctive, animal-vegetal polarity of distribution, their dramatic appearance during maturation, and their disapperance during activation are correlated with previously documented patterns of calcium-mediated events in anuran eggs. We discuss several lines of evidence supporting the hypothesis that these junctions in xenopus eggs are sites that transduce extracellular events into intracellular calcium release during fertilization and activation of development.

Dehydroepiandrosterone inhibits intracellular calcium release in β-cells by a plasma membrane-dependent mechanism

Steroids ◽  
2006 ◽  
Vol 71 (8) ◽  
pp. 691-699 ◽  
Author(s):  
Dongmin Liu ◽  
Min Ren ◽  
Xinyu Bing ◽  
Corey Stotts ◽  
Sundeep Deorah ◽  
...  
Keyword(s):  
Plasma Membrane ◽  
Intracellular Calcium ◽  
Calcium Release ◽  
Β Cells ◽  
Intracellular Calcium Release ◽  
Dependent Mechanism

scholarly journals The Builders of the Junction: Roles of Junctophilin1 and Junctophilin2 in the Assembly of the Sarcoplasmic Reticulum–Plasma Membrane Junctions in Striated Muscle

Biomolecules ◽  
2022 ◽  
Vol 12 (1) ◽  
pp. 109
Author(s):  
Stefano Perni
Keyword(s):  
Plasma Membrane ◽  
Sarcoplasmic Reticulum ◽  
Intracellular Calcium ◽  
Cardiac Muscle ◽  
Structure Prediction ◽  
Calcium Release ◽  
Striated Muscle ◽  
Short Review ◽  
Published Data ◽  
Intracellular Calcium Release

Contraction of striated muscle is triggered by a massive release of calcium from the sarcoplasmic reticulum (SR) into the cytoplasm. This intracellular calcium release is initiated by membrane depolarization, which is sensed by voltage-gated calcium channels CaV1.1 (in skeletal muscle) and CaV1.2 (in cardiac muscle) in the plasma membrane (PM), which in turn activate the calcium-releasing channel ryanodine receptor (RyR) embedded in the SR membrane. This cross-communication between channels in the PM and in the SR happens at specialized regions, the SR-PM junctions, where these two compartments come in close proximity. Junctophilin1 and Junctophilin2 are responsible for the formation and stabilization of SR-PM junctions in striated muscle and actively participate in the recruitment of the two essential players in intracellular calcium release, CaV and RyR. This short review focuses on the roles of junctophilins1 and 2 in the formation and organization of SR-PM junctions in skeletal and cardiac muscle and on the functional consequences of the absence or malfunction of these proteins in striated muscle in light of recently published data and recent advancements in protein structure prediction.

scholarly journals Junctate is a key element in calcium entry induced by activation of InsP3 receptors and/or calcium store depletion

2004 ◽  
Vol 166 (4) ◽  
pp. 537-548 ◽  
Author(s):  
Susan Treves ◽  
Clara Franzini-Armstrong ◽  
Luca Moccagatta ◽  
Christophe Arnoult ◽  
Cristiano Grasso ◽  
...  
Keyword(s):  
Plasma Membrane ◽  
Intracellular Calcium ◽  
Calcium Binding ◽  
Calcium Release ◽  
Transient Receptor Potential ◽  
Receptor Activation ◽  
Calcium Entry ◽  
Calcium Stores ◽  
Store Depletion ◽  
Insp3 Receptors

In many cell types agonist-receptor activation leads to a rapid and transient release of Ca2+ from intracellular stores via activation of inositol 1,4,5 trisphosphate (InsP3) receptors (InsP3Rs). Stimulated cells activate store- or receptor-operated calcium channels localized in the plasma membrane, allowing entry of extracellular calcium into the cytoplasm, and thus replenishment of intracellular calcium stores. Calcium entry must be finely regulated in order to prevent an excessive intracellular calcium increase. Junctate, an integral calcium binding protein of endo(sarco)plasmic reticulum membrane, (a) induces and/or stabilizes peripheral couplings between the ER and the plasma membrane, and (b) forms a supramolecular complex with the InsP3R and the canonical transient receptor potential protein (TRPC) 3 calcium entry channel. The full-length protein modulates both agonist-induced and store depletion–induced calcium entry, whereas its NH2 terminus affects receptor-activated calcium entry. RNA interference to deplete cells of endogenous junctate, knocked down both agonist-activated calcium release from intracellular stores and calcium entry via TRPC3. These results demonstrate that junctate is a new protein involved in calcium homeostasis in eukaryotic cells.

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