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Int. J. Mol. Sci. 2016, 17(12), 2097;

Differential Impacts of Alternative Splicing Networks on Apoptosis

School of Medical Laboratory Science and Biotechnology, College of Medical Science and Technology, Taipei Medical University, Taipei 11031, Taiwan
Department of Laboratory Medicine, Taipei Medical University Hospital, Taipei 11031, Taiwan
School of Chinese Medicine, China Medical University, Taichung 404, Taiwan
Author to whom correspondence should be addressed.
Academic Editors: Charles J. Malemud and Anthony Lemarié
Received: 14 October 2016 / Revised: 26 November 2016 / Accepted: 2 December 2016 / Published: 14 December 2016
(This article belongs to the Collection Programmed Cell Death and Apoptosis)
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Apoptosis functions as a common mechanism to eliminate unnecessary or damaged cells during cell renewal and tissue development in multicellular organisms. More than 200 proteins constitute complex networks involved in apoptotic regulation. Imbalanced expressions of apoptosis-related factors frequently lead to malignant diseases. The biological functions of several apoptotic factors are manipulated through alternative splicing mechanisms which expand gene diversity by generating discrete variants from one messenger RNA precursor. It is widely observed that alternatively-spliced variants encoded from apoptosis-related genes exhibit differential effects on apoptotic regulation. Alternative splicing events are meticulously regulated by the interplay between trans-splicing factors and cis-responsive elements surrounding the regulated exons. The major focus of this review is to highlight recent studies that illustrate the influences of alternative splicing networks on apoptotic regulation which participates in diverse cellular processes and diseases. View Full-Text
Keywords: alternative splicing; apoptosis; organogenesis; carcinogenesis alternative splicing; apoptosis; organogenesis; carcinogenesis

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Lin, J.-C.; Tsao, M.-F.; Lin, Y.-J. Differential Impacts of Alternative Splicing Networks on Apoptosis. Int. J. Mol. Sci. 2016, 17, 2097.

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