Vulnerability of Store-Operated Calcium Entry to Inhibitors and Microenvironment in Cells of Different Breast Cancer Subtypes.

The incidence and development of cancer are highly dependent on pathological disturbances in calcium homeostasis of the cell. One of the major pathways for calcium entry is store-operated calcium entry (SOCE), which functions in virtually all cell types. Changes in the expression level of the main proteins organizing SOCE are observed during the development of various cancer types, particularly breast cancer (BC).

Reorganization and Suppression of Store-Operated Calcium Entry in Podocytes of Type 2 Diabetic Rats.

Type 2 diabetes mellitus (DM2) is a widespread metabolic disorder that results in podocyte damage and diabetic nephropathy. Previous studies demonstrated that TRPC6 channels play a pivotal role in podocyte function and their dysregulation is associated with development of different kidney diseases including nephropathy. Here, using single channel patch clamp technique, we demonstrated that non-selective cationic TRPC6 channels are sensitive to the Ca store depletion in human podocyte cell line Ab8/13 and in freshly isolated rat glomerular podocytes.

Role of STIM2 and Orai proteins in regulating TRPC1 channel activity upon calcium store depletion.

Store-operated calcium channels are the major player in calcium signaling in non-excitable cells. Store-operated calcium entry is associated with the Orai, stromal interaction molecule (STIM), and transient receptor potential canonical (TRPC) protein families. Researchers have provided conflicting data about TRPC1 channel regulation by Orai and STIM.

A Novel Modulator of STIM2-Dependent Store-Operated Ca2+ Channel Activity.

Store-operated Ca entry is one of the main pathways of calcium influx into non-excitable cells, which entails the initiation of many intracellular processes. The endoplasmic reticulum Ca sensors STIM1 and STIM2 are the key components of store-operated Ca entry in mammalian cells. Under physiological conditions, STIM proteins are responsible for store-operated Ca entry activation.

Electrophysiological Properties of Endogenous Single Ca Activated Cl Channels Induced by Local Ca Entry in HEK293.

Microdomains formed by proteins of endoplasmic reticulum and plasma membrane play a key role in store-operated Ca entry (SOCE). Ca release through inositol 1,4,5-trisphosphate receptor (IPR) and subsequent Ca store depletion activate STIM (stromal interaction molecules) proteins, sensors of intraluminal Ca, which, in turn, open the Orai channels in plasma membrane. Downstream to this process could be activated TRPC (transient receptor potential-canonical) calcium permeable channels.