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@article{Ghiasi:2021:10.3389/fendo.2021.625235,
author = {Ghiasi, SM and Rutter, GA},
doi = {10.3389/fendo.2021.625235},
journal = {Frontiers in Endocrinology},
pages = {1--12},
title = {Consequences for pancreatic beta-cell identity and function of unregulated transcript processing},
url = {http://dx.doi.org/10.3389/fendo.2021.625235},
volume = {12},
year = {2021}
}

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TY  - JOUR
AB  - Mounting evidence suggests a role for alternative splicing (AS) of transcripts in the normal physiology and pathophysiology of the pancreatic β-cell. In the apparent absence of RNA repair systems, RNA decay pathways are likely to play an important role in controlling the stability, distribution and diversity of transcript isoforms in these cells. Around 35% of alternatively spliced transcripts in human cells contain premature termination codons (PTCs) and are targeted for degradation via nonsense-mediated decay (NMD), a vital quality control process. Inflammatory cytokines, whose levels are increased in both type 1 (T1D) and type 2 (T2D) diabetes, stimulate alternative splicing events and the expression of NMD components, and may or may not be associated with the activation of the NMD pathway. It is, however, now possible to infer that NMD plays a crucial role in regulating transcript processing in normal and stress conditions in pancreatic β-cells. In this review, we describe the possible role of Regulated Unproductive Splicing and Translation (RUST), a molecular mechanism embracing NMD activity in relationship to AS and translation of damaged transcript isoforms in these cells. This process substantially reduces the abundance of non-functional transcript isoforms, and its dysregulation may be involved in pancreatic β-cell failure in diabetes.
AU  - Ghiasi,SM
AU  - Rutter,GA
DO  - 10.3389/fendo.2021.625235
EP  - 12
PY  - 2021///
SN  - 1664-2392
SP  - 1
TI  - Consequences for pancreatic beta-cell identity and function of unregulated transcript processing
T2  - Frontiers in Endocrinology
UR  - http://dx.doi.org/10.3389/fendo.2021.625235
UR  - http://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcApp=PARTNER_APP&SrcAuth=LinksAMR&KeyUT=WOS:000631173700001&DestLinkType=FullRecord&DestApp=ALL_WOS&UsrCustomerID=1ba7043ffcc86c417c072aa74d649202
UR  - https://www.frontiersin.org/articles/10.3389/fendo.2021.625235/full
UR  - http://hdl.handle.net/10044/1/87783
VL  - 12
ER  -

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