Blockade of Ca3 calcium channels and induction of G/G cell cycle arrest in colon cancer cells by gossypol.

Background And Purpose: Gastrointestinal tumours overexpress voltage-gated calcium (Ca3) channels (Ca3.1, 3.2 and 3.

Heterogeneity of the endoplasmic reticulum Ca store determines colocalization with mitochondria.

Contact sites between the endoplasmic reticulum (ER) and mitochondria play a pivotal role in cell signaling, and the interaction between these organelles is dynamic and finely regulated. We have studied the role of ER Ca concentration ([Ca]) in modulating this association in HeLa and HEK293 cells and human fibroblasts. According to Manders' coefficient, ER-mitochondria colocalization varied depending on the ER marker; it was the highest with ER-Tracker and the lowest with ER Ca indicators (Mag-Fluo-4, erGAP3, and G-CEPIA1er) in both HeLa cells and human fibroblasts.

PKC Inhibits Sec61 Translocon-Mediated Sarcoplasmic Reticulum Ca Leak in Smooth Muscle Cells.

PKC inhibitors stimulate Ca release from internal stores in diverse cell types. Our data indicate that this action cannot be explained by an increased agonist-induced IP production or an overloaded SR Ca pool in smooth muscle cells from guinea pig urinary bladder. The incubation of these cells with three different PKC inhibitors, such as Go6976, Go6983, and BIM 1, resulted in a higher SR Ca leak revealed by inhibition of the SERCA pump with thapsigargin.

Aldosterone-Induced Sarco/Endoplasmic Reticulum Ca Pump Upregulation Counterbalances Ca1.2-Mediated Ca Influx in Mesenteric Arteries.

In mesenteric arteries (MAs), aldosterone (ALDO) binds to the endogenous mineralocorticoid receptor (MR) and increases the expression of the voltage-gated L-type Ca1.2 channel, an essential ion channel for vascular contraction, sarcoplasmic reticulum (SR) Ca store refilling, and Ca spark generation. In mesenteric artery smooth muscle cells (MASMCs), Ca influx through Ca1.