Distinct Gene Expression Patterns of Calcium Channels and Related Signaling Pathways Discovered in Lymphomas.

Cell surface calcium (Ca) channels permit Ca ion influx, with Ca taking part in cellular functions such as proliferation, survival, and activation. The expression of voltage-dependent Ca (Ca) channels may modulate the growth of hematologic cancers. Profile analysis of Ca channels, with a focus on the Ca release-activated Ca (CRAC) and L-type Ca channels, was performed on RNA sequencing data from lymphoma cell lines and samples derived from patients with diffuse large B cell lymphoma (DLBCL).

Mutation of an L-Type Calcium Channel Gene Leads to T Lymphocyte Dysfunction.

Calcium (Ca) is a vital secondary messenger in T lymphocytes regulating a vast array of important events including maturation, homeostasis, activation, and apoptosis and can enter the cell through CRAC, TRP, and Ca channels. Here we describe a mutation in the L-type Ca channel Ca1.4 leading to T lymphocyte dysfunction, including several hallmarks of immunological exhaustion.

The 13th Annual Aurora Biomed Ion Channel Retreat: Three Days of Research, Technology, and Networking.

The 13th Annual Ion Channel Retreat was held by Aurora Biomed in Vancouver, Canada from July 7 to 9, 2015. The meeting showcased prominent current research including cardiac safety and pharmacology; ion channel structure, function and engineering; transporters and ion pumps; screening technologies; ion channels as disease targets; alcohol, tobacco, and ion channels; and ion channels as pain targets. This report summarizes the work presented at the retreat.

Tweeters, Woofers and Horns: The Complex Orchestration of Calcium Currents in T Lymphocytes.

Elevation of intracellular calcium ion (Ca(2+)) levels is a vital event that regulates T lymphocyte homeostasis, activation, proliferation, differentiation, and apoptosis. The mechanisms that regulate intracellular Ca(2+) signaling in lymphocytes involve tightly controlled concinnity of multiple ion channels, membrane receptors, and signaling molecules. T cell receptor (TCR) engagement results in depletion of endoplasmic reticulum (ER) Ca(2+) stores and subsequent sustained influx of extracellular Ca(2+) through Ca(2+) release-activated Ca(2+) (CRAC) channels in the plasma membrane.

The ion channel TRPV1 regulates the activation and proinflammatory properties of CD4⁺ T cells.

TRPV1 is a Ca(2+)-permeable channel studied mostly as a pain receptor in sensory neurons. However, its role in other cell types is poorly understood. Here we found that TRPV1 was functionally expressed in CD4(+) T cells, where it acted as a non-store-operated Ca(2+) channel and contributed to T cell antigen receptor (TCR)-induced Ca(2+) influx, TCR signaling and T cell activation.