Voltage-Gated T-Type Calcium Channel Modulation by Kinases and Phosphatases: The Old Ones, the New Ones, and the Missing Ones

Bhargava, Anamika (2023) Voltage-Gated T-Type Calcium Channel Modulation by Kinases and Phosphatases: The Old Ones, the New Ones, and the Missing Ones. Cells, 12 (3). p. 461. ISSN 2073-4409

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Abstract

Calcium (Ca2+) can regulate a wide variety of cellular fates, such as proliferation, apoptosis, and autophagy. More importantly, changes in the intracellular Ca2+ level can modulate signaling pathways that control a broad range of physiological as well as pathological cellular events, including those important to cellular excitability, cell cycle, gene-transcription, contraction, cancer progression, etc. Not only intracellular Ca2+ level but the distribution of Ca2+ in the intracellular compartments is also a highly regulated process. For this Ca2+ homeostasis, numerous Ca2+ chelating, storage, and transport mechanisms are required. There are also specialized proteins that are responsible for buffering and transport of Ca2+. T-type Ca2+ channels (TTCCs) are one of those specialized proteins which play a key role in the signal transduction of many excitable and non-excitable cell types. TTCCs are low-voltage activated channels that belong to the family of voltage-gated Ca2+ channels. Over decades, multiple kinases and phosphatases have been shown to modulate the activity of TTCCs, thus playing an indirect role in maintaining cellular physiology. In this review, we provide information on the kinase and phosphatase modulation of TTCC isoforms Cav3.1, Cav3.2, and Cav3.3, which are mostly described for roles unrelated to cellular excitability. We also describe possible potential modulations that are yet to be explored. For example, both mitogen-activated protein kinase and citron kinase show affinity for different TTCC isoforms; however, the effect of such interaction on TTCC current/kinetics has not been studied yet.

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IITH Creators:

IITH Creators	ORCiD
Bhargava, Anamika	http://orcid.org/0000-0002-1048-3427

Item Type:

Article

Uncontrolled Keywords:

calcium; kinase; modulation; phosphatase; T-type calcium channels; acetylcholine; beta catenin; calcineurin; calcium calmodulin dependent protein kinase II; calcium channel T type; cannabinoid receptor; cav3 1 calcium channel; cav3 2 calcium channel; cav3 3 calcium channel; connexin 43; cyclic AMP dependent protein kinase; cyclic GMP dependent protein kinase; cyclin dependent kinase 5; cystathionine gamma lyase; fibroblast growth factor 1; fibroblast growth factor 23; high mobility group B1 protein; hypoxia inducible factor 1alpha; melatonin; mitogen activated protein kinase; phorbol 13 acetate 12 myristate; phosphatase; phosphatidylinositol 3,4,5 trisphosphate 3 phosphatase; phosphoprotein phosphatase; protein kinase; Rho kinase; snake venom; unclassified drug; vincristine; voltage gated calcium channel; apoptosis; astrocyte; autophagy (cellular); cancer growth; cell cycle; cell cycle G2 phase; cell cycle M phase; cell proliferation; cognitive defect; excitability; gene overexpression; genetic transcription; homeostasis; human; hypertension; ion transport; nonhuman; phosphorylation; physiology; protein degradation; renin angiotensin aldosterone system; Review

Subjects:

Others > Biotechnology

Divisions:

Department of Biotechnology

Depositing User:

Mr Nigam Prasad Bisoyi

Date Deposited:

18 Aug 2023 11:58

Last Modified:

18 Aug 2023 11:58

URI:

http://raiithold.iith.ac.in/id/eprint/11574