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Alternative Splicing of L-type CaV1.2 Calcium Channels: Implications in Cardiovascular Diseases

1
Department of Physiology, Yong Loo Lin School of Medicine, National University of Singapore, Singapore 117593, Singapore
2
Neurobiology/Ageing Programme, Center for Life Sciences, NUS Graduate School for Integrative Sciences and Engineering, Singapore 117456, Singapore
3
Neurobiology/Ageing Programme, Center for Life Sciences, National University of Singapore, Singapore 117456, Singapore
*
Author to whom correspondence should be addressed.
Genes 2017, 8(12), 344; https://doi.org/10.3390/genes8120344
Received: 11 October 2017 / Revised: 9 November 2017 / Accepted: 21 November 2017 / Published: 24 November 2017
(This article belongs to the Special Issue Aberrant Pre-mRNA Splicing in Disease)
L-type CaV1.2 calcium channels are the major pathway for Ca2+ influx to initiate the contraction of smooth and cardiac muscles. Alteration of CaV1.2 channel function has been implicated in multiple cardiovascular diseases, such as hypertension and cardiac hypertrophy. Alternative splicing is a post-transcriptional mechanism that expands CaV1.2 channel structures to modify function, pharmacological and biophysical property such as calcium/voltage-dependent inactivation (C/VDI), or to influence its post-translational modulation by interacting proteins such as Galectin-1. Alternative splicing has generated functionally diverse CaV1.2 isoforms that can be developmentally regulated in the heart, or under pathophysiological conditions such as in heart failure. More importantly, alternative splicing of certain exons of CaV1.2 has been reported to be regulated by splicing factors such as RNA-binding Fox-1 homolog 1/2 (Rbfox 1/2), polypyrimidine tract-binding protein (PTBP1) and RNA-binding motif protein 20 (RBM20). Understanding how CaV1.2 channel function is remodelled in disease will provide better information to guide the development of more targeted approaches to discover therapeutic agents for cardiovascular diseases. View Full-Text
Keywords: L-type CaV1.2 calcium channel; alternative splicing; cardiovascular diseases L-type CaV1.2 calcium channel; alternative splicing; cardiovascular diseases
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MDPI and ACS Style

Hu, Z.; Liang, M.C.; Soong, T.W. Alternative Splicing of L-type CaV1.2 Calcium Channels: Implications in Cardiovascular Diseases. Genes 2017, 8, 344. https://doi.org/10.3390/genes8120344

AMA Style

Hu Z, Liang MC, Soong TW. Alternative Splicing of L-type CaV1.2 Calcium Channels: Implications in Cardiovascular Diseases. Genes. 2017; 8(12):344. https://doi.org/10.3390/genes8120344

Chicago/Turabian Style

Hu, Zhenyu, Mui C. Liang, and Tuck W. Soong 2017. "Alternative Splicing of L-type CaV1.2 Calcium Channels: Implications in Cardiovascular Diseases" Genes 8, no. 12: 344. https://doi.org/10.3390/genes8120344

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