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Differential Impacts of Alternative Splicing Networks on Apoptosis

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 frequent...

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Detalles Bibliográficos
Autores principales: Lin, Jung-Chun, Tsao, Mei-Fen, Lin, Ying-Ju
Formato: Online Artículo Texto
Lenguaje:English
Publicado: MDPI 2016
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5187897/
https://www.ncbi.nlm.nih.gov/pubmed/27983653
http://dx.doi.org/10.3390/ijms17122097
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author Lin, Jung-Chun
Tsao, Mei-Fen
Lin, Ying-Ju
author_facet Lin, Jung-Chun
Tsao, Mei-Fen
Lin, Ying-Ju
author_sort Lin, Jung-Chun
collection PubMed
description 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.
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spelling pubmed-51878972016-12-30 Differential Impacts of Alternative Splicing Networks on Apoptosis Lin, Jung-Chun Tsao, Mei-Fen Lin, Ying-Ju Int J Mol Sci Review 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. MDPI 2016-12-14 /pmc/articles/PMC5187897/ /pubmed/27983653 http://dx.doi.org/10.3390/ijms17122097 Text en © 2016 by the authors; licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC-BY) license (http://creativecommons.org/licenses/by/4.0/).
spellingShingle Review
Lin, Jung-Chun
Tsao, Mei-Fen
Lin, Ying-Ju
Differential Impacts of Alternative Splicing Networks on Apoptosis
title Differential Impacts of Alternative Splicing Networks on Apoptosis
title_full Differential Impacts of Alternative Splicing Networks on Apoptosis
title_fullStr Differential Impacts of Alternative Splicing Networks on Apoptosis
title_full_unstemmed Differential Impacts of Alternative Splicing Networks on Apoptosis
title_short Differential Impacts of Alternative Splicing Networks on Apoptosis
title_sort differential impacts of alternative splicing networks on apoptosis
topic Review
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5187897/
https://www.ncbi.nlm.nih.gov/pubmed/27983653
http://dx.doi.org/10.3390/ijms17122097
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