Voltage-dependent L-type calcium channel subunit alpha-1C

Definition:

Pore-forming, alpha-1C subunit of the voltage-gated calcium channel that gives rise to L-type calcium currents. Mediates influx of calcium ions into the cytoplasm, and thereby triggers calcium release from the sarcoplasm (By similarity). Plays an important role in excitation-contraction coupling in the heart. Required for normal heart development and normal regulation of heart rhythm. Required for normal contraction of smooth muscle cells in blood vessels and in the intestine. Essential for normal blood pressure regulation via its role in the contraction of arterial smooth muscle cells. Long-lasting (L-type) calcium channels belong to the 'high-voltage activated' (HVA) group (Probable).; (Microbial infection) Acts as a receptor for Influenzavirus. May play a critical role in allowing virus entry when sialylated and expressed on lung tissues.

References:

[1]. N M Soldatov, et al. Molecular structures involved in L-type calcium channel inactivation. Role of the carboxyl-terminal region encoded by exons 40-42 in alpha1C subunit in the kinetics and Ca2+ dependence of inactivation. J Biol Chem. 1997 Feb 7;272(6):3560-6. [Content Brief]

[2]. Nicole J Boczek, et al. Identification and Functional Characterization of a Novel CACNA1C-Mediated Cardiac Disorder Characterized by Prolonged QT Intervals With Hypertrophic Cardiomyopathy, Congenital Heart Defects, and Sudden Cardiac Death. Circ Arrhythm Electrophysiol. 2015 Oct;8(5):1122-32. [Content Brief]

[3]. Igor Splawski, et al. Ca(V)1.2 calcium channel dysfunction causes a multisystem disorder including arrhythmia and autism. Cell. 2004 Oct 1;119(1):19-31. [Content Brief]

[4]. Megumi Fukuyama, et al. Long QT syndrome type 8: novel CACNA1C mutations causing QT prolongation and variant phenotypes. Europace. 2014 Dec;16(12):1828-37. [Content Brief]

[5]. N M Soldatov, et al. Different voltage-dependent inhibition by dihydropyridines of human Ca2+ channel splice variants. J Biol Chem. 1995 May 5;270(18):10540-3. [Content Brief]

[6]. Eun Young Kim, et al. Multiple C-terminal tail Ca(2+)/CaMs regulate Ca(V)1.2 function but do not mediate channel dimerization. EMBO J. 2010 Dec 1;29(23):3924-38. [Content Brief]

[7]. Ning Qin, et al. Molecular cloning and characterization of the human voltage-gated calcium channel alpha(2)delta-4 subunit. Mol Pharmacol. 2002 Sep;62(3):485-96. [Content Brief]

[8]. Greg L Lyford, et al. alpha(1C) (Ca(V)1.2) L-type calcium channel mediates mechanosensitive calcium regulation. Am J Physiol Cell Physiol. 2002 Sep;283(3):C1001-8. [Content Brief]

[9]. Peter Bartels, et al. Alternative Splicing at N Terminus and Domain I Modulates CaV1.2 Inactivation and Surface Expression. Biophys J. 2018 May 8;114(9):2095-2106. [Content Brief]

[10]. S Tang, et al. Molecular localization of ion selectivity sites within the pore of a human L-type cardiac calcium channel. J Biol Chem. 1993 Jun 25;268(18):13026-9. [Content Brief]

[11]. Yakov Blumenstein, et al. A novel long N-terminal isoform of human L-type Ca2+ channel is up-regulated by protein kinase C. J Biol Chem. 2002 Feb 1;277(5):3419-23. [Content Brief]

[12]. U Klöckner, et al. Properties of three COOH-terminal splice variants of a human cardiac L-type Ca2+-channel alpha1-subunit. Am J Physiol. 1997 Mar;272(3 Pt 2):H1372-81. [Content Brief]

[13]. Igor Splawski, et al. Severe arrhythmia disorder caused by cardiac L-type calcium channel mutations. Proc Natl Acad Sci U S A. 2005 Jun 7;102(23):8089-96; discussion 8086-8. [Content Brief]

[14]. Swasti Tiwari, et al. Atherosclerosis-related molecular alteration of the human CaV1.2 calcium channel alpha1C subunit. Proc Natl Acad Sci U S A. 2006 Nov 7;103(45):17024-9. [Content Brief]

[15]. Siobhan M Wong King Yuen, et al. Structural insights into binding of STAC proteins to voltage-gated calcium channels. Proc Natl Acad Sci U S A. 2017 Nov 7;114(45):E9520-E9528. [Content Brief]

[16]. Brittan S Sutphin, et al. Molecular and Functional Characterization of Rare CACNA1C Variants in Sudden Unexplained Death in the Young. Congenit Heart Dis. 2016 Dec;11(6):683-692. [Content Brief]

[17]. R D Zühlke, et al. Ca2+ channel sensitivity towards the blocker isradipine is affected by alternative splicing of the human alpha1C subunit gene. FEBS Lett. 1998 May 8;427(2):220-4. [Content Brief]

[18]. Filip Van Petegem, et al. Insights into voltage-gated calcium channel regulation from the structure of the CaV1.2 IQ domain-Ca2+/calmodulin complex. Nat Struct Mol Biol. 2005 Dec;12(12):1108-15. [Content Brief]

[19]. Yoichiro Fujioka, et al. A Sialylated Voltage-Dependent Ca2+ Channel Binds Hemagglutinin and Mediates Influenza A Virus Entry into Mammalian Cells. Cell Host Microbe. 2018 Jun 13;23(6):809-818.e5. [Content Brief]

[20]. Matthew A Nystoriak, et al. Ser1928 phosphorylation by PKA stimulates the L-type Ca2+ channel CaV1.2 and vasoconstriction during acute hyperglycemia and diabetes. Sci Signal. 2017 Jan 24;10(463):eaaf9647. [Content Brief]

[21]. D Schultz, et al. Cloning, chromosomal localization, and functional expression of the alpha 1 subunit of the L-type voltage-dependent calcium channel from normal human heart. Proc Natl Acad Sci U S A. 1993 Jul 1;90(13):6228-32. [Content Brief]

[22]. Nicole J Boczek, et al. Exome sequencing and systems biology converge to identify novel mutations in the L-type calcium channel, CACNA1C, linked to autosomal dominant long QT syndrome. Circ Cardiovasc Genet. 2013 Jun;6(3):279-89. [Content Brief]

[23]. Charles Antzelevitch, et al. Loss-of-function mutations in the cardiac calcium channel underlie a new clinical entity characterized by ST-segment elevation, short QT intervals, and sudden cardiac death. Circulation. 2007 Jan 30;115(4):442-9. [Content Brief]

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