Please use this identifier to cite or link to this item: http://scholarbank.nus.edu.sg/handle/10635/143318
Title: ALTERNATIVE SPLICING AND GALECTIN-1 MODULATE L-TYPE CAV1.2 CALCIUM CHANNEL FUNCTION: IMPLICATIONS IN CARDIOVASCULAR DISEASES
Authors: ZHENYU HU
Keywords: Cav1.2 channel, alternative splicing, Galectin-1, proteasomal degradation, hypertension
Issue Date: 13-Jan-2017
Citation: ZHENYU HU (2017-01-13). ALTERNATIVE SPLICING AND GALECTIN-1 MODULATE L-TYPE CAV1.2 CALCIUM CHANNEL FUNCTION: IMPLICATIONS IN CARDIOVASCULAR DISEASES. ScholarBank@NUS Repository.
Abstract: L-type voltage-gated Cav1.2 calcium channel is the primary pathway for calcium influx in heart and smooth muscle. The two primary aims of the present thesis were to functionally characterize a newly identified cardiac hypertrophy-related Cav1.2 splice variant, Cav1.2-e21+22 that includes both exons 21 and 22 and to validate the roles of a novel Cav1.2-interacting partner, Galectin-1, in regulation of blood pressure. In Chapter II, we mainly showed that Cav1.2-e21+22 functioned as a Cavβ trap and thereby induced wild-type Cav1.2 degradation due to lack of Cavβ. In Chapter III, we showed that Galectin-1 reduced Cav1.2 protein level by enhancing poly-ubiquitination of lysines embedded within Cav1.2 I-II loop that subsequently led to degradation via the ubiquitin-proteasome system. Significantly, targeting Galectin-1 by either over-expression in blood vessels or by Tat-e9c peptide infusion to specifically disrupt Cav1.2-Galectin-1 interaction was potentially a direct and efficient approach to regulate blood pressure.
URI: http://scholarbank.nus.edu.sg/handle/10635/143318
Appears in Collections:Ph.D Theses (Open)

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