| Literature DB >> 32767122 |
Marie Potier-Cartereau1, William Raoul1, Gunther Weber1, Karine Mahéo1, Raphael Rapetti-Mauss2, Maxime Gueguinou3, Paul Buscaglia4, Caroline Goupille5, Nelig Le Goux4, Souleymane Abdoul-Azize4, Thierry Lecomte6, Gaëlle Fromont7, Aurélie Chantome1, Olivier Mignen4, Olivier Soriani2, Christophe Vandier8.
Abstract
The intracellular Ca2+ concentration is mainly controlled by Ca2+ channels. These channels form complexes with K+ channels, which function to amplify Ca2+ flux. In cancer cells, voltage-gated/voltage-dependent Ca2+ channels and non-voltage-gated/voltage-independent Ca2+ channels have been reported to interact with K+ channels such as Ca2+-activated K+ channels and voltage-gated K+ channels. These channels are activated by an increase in cytosolic Ca2+ concentration or by membrane depolarization, which induces membrane hyperpolarization, increasing the driving force for Ca2+ flux. These complexes, composed of K+ and Ca2+ channels, are regulated by several molecules including lipids (ether lipids and cholesterol), proteins (e.g. STIM), receptors (e.g. S1R/SIGMAR1), and peptides (e.g. LL-37) and can be targeted by monoclonal antibodies, making them novel targets for cancer research.Entities:
Keywords: Ca2+ channels; Cancer; K+ channels; LL-37; Lipids; SIGMAR1; STIM
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Year: 2022 PMID： 32767122 DOI： 10.1007/112_2020_24
Source DB: PubMed Journal: Rev Physiol Biochem Pharmacol ISSN： 0303-4240 Impact factor: 5.545