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Ion Channels in Immune Cells
Published in Shyam S. Bansal, Immune Cells, Inflammation, and Cardiovascular Diseases, 2022
Devasena Ponnalagu, Shridhar Sanghvi, Shyam S. Bansal, Harpreet Singh
CLICs autoinsert into lipid membranes and function as ion channels142,143. The transition from soluble to integral membrane form requires structural rearrangements in the protein, but the exact mechanism has not yet been deciphered. The most studied CLIC in terms of channel activity is CLIC1. It has been shown that the channel activity of CLIC1 is pH dependent144,145. The conformational stability of the CLIC1 protein was found to be altered at lower pH, as it was observed that CLIC forms partially unfolded intermediates that increase further upon low pH146 and thereby help in its autoinsertion. The N-terminal sequence between C24 and V46, comprising the putative transmembrane (PTM) domain, has been shown to form a helical structure both at pH 7.4 and at a lower pH of 5.0146. It was also shown that the mutation of PTM residue C24 resulted in the inhibition of channel activity, but the channel insertion or formation was not affected147.
Common sleep disorders
Published in Ravi Gupta, S. R. Pandi Perumal, Ahmed S. BaHammam, Clinical Atlas of Polysomnography, 2018
Ravi Gupta, S. R. Pandi Perumal, Ahmed S. BaHammam
Gurski, L. A., Knowles, L. M., Basse, P. H., Maranchie, J. K., Watkins, S. C., & Pilch, J., (2015). Relocation of CLIC1 promotes tumor cell invasion and colonization of fibrin. Mol Cancer Res. 13(2), 273-280.
The protective effect of tanshinone IIa on endothelial cells: a generalist among clinical therapeutics
Published in Expert Review of Clinical Pharmacology, 2021
Jun Feng, Lina Liu, Fangfang Yao, Daixing Zhou, Yang He, Junshuai Wang
Intracellular chloride channel 1 (CLIC1), a unique chloride ion channel related to macrophage activation is both a sensor and an effector under oxidative stress and plays the primary role in diseases involving oxidative stress, such as tumors and neurodegenerative diseases, by regulating cell adhesion, cell cycle, apoptosis, and promotion of metastasis in tumor progression [79]. STS could induce Cl−secretion by CaCC in a mAChR-dependent manner to modulate ion transport in airway epithelial cells for the hydration of airways [80]. STS-induced dose-dependent relaxation of mouse tracheal rings in an epithelial cell-independent manner. STS also decreased CLIC1 expression, reduced lipid peroxidation, promoted antioxidant defensive systems and inflammatory levels, and resulted in a beneficial effect on anti-atherosclerosis [81]. These studies support the development and application of STS to affect vascular tone in pathological conditions, such as improving coronary blood flow in coronary heart disease.
Chloride intracellular channel protein 2 in cancer and non-cancer human tissues: relationship with tight junctions
Published in Tissue Barriers, 2019
Yoshitomo Ueno, Saya Ozaki, Akihiro Umakoshi, Hajime Yano, Mohammed E. Choudhury, Naoki Abe, Yutaro Sumida, Jun Kuwabara, Rina Uchida, Afsana Islam, Kohei Ogawa, Kei Ishimaru, Toshihiro Yorozuya, Takeharu Kunieda, Yuji Watanabe, Yasutsugu Takada, Junya Tanaka
Chloride intracellular channel proteins (CLICs) were recently identified, and currently six related human genes encoding CLIC1–6 have been reported1,2 Because CLIC proteins are highly conserved throughout metazoa, they are thought to play critical roles in maintaining life3,4 Although they are considered multifunctional proteins, the common functions of CLICs have not been well defined5 When inserted into an artificial lipid bilayer, they formed chloride ion channels6,7 However, most cellular CLICs are not present as membrane-bound proteins but as soluble proteins or localized in cell nuclei. The intimate interactions of CLICs with the actin cytoskeleton have been frequently reported, suggesting pivotal roles in the regulation of cytoskeletal organization6,8,9 Nuclear CLIC4 may be involved in transforming growth factor β (TGFβ)-mediated signaling. Studies of CLIC4-null mice indicated CLIC4 might be involved in renal tubulogenesis10 CLIC1-null mice had impaired phagosome acidification, which caused the dysfunction of macrophages, which expressed CLIC1 at a high level in normal animals11 Jitterbug mice have a natural mutation in the clic5 gene and have impaired hearing and balance12 Many other functions of CLICs have been reported and therefore it is difficult to determine the specific nature and roles of CLICs. Identifying which proteins or factors interact with CLICs might help elucidate their roles; however, traditional methods such as immunoprecipitation or cross-linking techniques have not produced significant results1