English (United Kingdom)

https://curated-unify.zendy.io/wp-json/zendy-region/v1/featured_content/oa?rat=en

https://curated-unify.zendy.io/wp-json/zendy-region/v1/highlighted_journal/

Global: Zendy Plus annual

Presents the access of premium content as premium feature

Premium Content

Presents the keyphrase highlighting as premium feature

Keyphrase Highlighting

Presents the summarisation as premium feature

Summarisation

Insights

Presents the pdf analysis as premium feature

PDF Analysis

Presents the zaia usage as premium feature

ZAIA

Global: Zendy Plus monthly

Global: Zendy Tools annual

Global: Zendy Tools monthly

Global: Zendy Free Plan

The role of voltage-dependent calcium (Cav1) channels is prominent in excitable cells while store-operated calcium channels (SOCC) were considered as characteristic of non-excitable cells. Cav1 channels are implicated in excitation transcription. Store-operated calcium channels (SOCC) activity is increased during cardiac stress and would contribute to Ca2+ influx and expression of genes responsible for cardiac hypertrophy and heart failure (Luo et al., 2012). Several lines of evidence now show the importance of Cav1 channels in non-excitable cells including lymphocytes (reviewed in Robert et al., 2011, 2013). Cav1 channels are defined by their voltage sensitivity and their sensitivity to drugs as dihydropyridines, phenylalkylamines, benzothiazepines, known to alter T-cell functions. However the drug concentrations needed were higher compared to excitable cells. The absence of cell membrane depolarization upon activation and possible non-specific effects of the drugs questioned the putative role of Cav1 channels in T-cells.  Cav1 channels are formed by the ion forming pore α1 subunit encoded by four genes conferring some tissue-specific expression pattern in excitable cells. Cav1.1 is characteristic of skeletal muscle cells. Cav1.2 is found in neurons, heart, and smooth muscle cells while Cav1.3 is detected in neuroendocrine cells. Cav1.2 and Cav1.3 can be found in the same tissues even if their role is not redundant as shown by the differential phenotypes of Cav1.2 and Cav1.3 null mice. Cav1.4 is the retinal form. Cav1 channel isoforms differ by their sensitivity to depolarization and to antagonizing drugs such as dihydropyridines (DHP) as well as by their inactivation properties (Lipscombe et al., 2004). For example, Cav1.4 channels activate at more negative potentials than Cav1.3 and Cav1.2, which highlights the potential involvement of Cav1.4 in non-excitable cells as mast cells (McRory et al., 2004) and more recently in mouse T-lymphocytes (Omilusik et al., 2011).

Ca2+ Signaling in T-Cell Subsets with a Focus on the Role of Cav1 Channels: Possible Implications in Therapeutics