The PARN, TOE1, and USB1 RNA deadenylases and their roles in non-coding RNA regulation.
PARN
TOE1
USB1
deadenylases
non-coding RNA regulation
Journal
The Journal of biological chemistry
ISSN: 1083-351X
Titre abrégé: J Biol Chem
Pays: United States
ID NLM: 2985121R
Informations de publication
Date de publication:
09 2023
09 2023
Historique:
received:
13
05
2023
revised:
28
07
2023
accepted:
29
07
2023
medline:
23
10
2023
pubmed:
7
8
2023
entrez:
6
8
2023
Statut:
ppublish
Résumé
The levels of non-coding RNAs (ncRNAs) are regulated by transcription, RNA processing, and RNA degradation pathways. One mechanism for the degradation of ncRNAs involves the addition of oligo(A) tails by non-canonical poly(A) polymerases, which then recruit processive sequence-independent 3' to 5' exonucleases for RNA degradation. This pathway of decay is also regulated by three 3' to 5' exoribonucleases, USB1, PARN, and TOE1, which remove oligo(A) tails and thereby can protect ncRNAs from decay in a manner analogous to the deubiquitination of proteins. Loss-of-function mutations in these genes lead to premature degradation of some ncRNAs and lead to specific human diseases such as Poikiloderma with Neutropenia (PN) for USB1, Dyskeratosis Congenita (DC) for PARN and Pontocerebellar Hypoplasia type 7 (PCH7) for TOE1. Herein, we review the biochemical properties of USB1, PARN, and TOE1, how they modulate ncRNA levels, and their roles in human diseases.
Identifiants
pubmed: 37544646
pii: S0021-9258(23)02167-1
doi: 10.1016/j.jbc.2023.105139
pmc: PMC10493513
pii:
doi:
Substances chimiques
Exoribonucleases
EC 3.1.-
RNA, Untranslated
0
TOE1 protein, human
0
USB1 protein, human
EC 3.1.4.-
poly(A)-specific ribonuclease
EC 3.1.13.4
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Research Support, U.S. Gov't, Non-P.H.S.
Review
Langues
eng
Sous-ensembles de citation
IM
Pagination
105139Subventions
Organisme : Howard Hughes Medical Institute
Pays : United States
Informations de copyright
Copyright © 2023 The Authors. Published by Elsevier Inc. All rights reserved.
Déclaration de conflit d'intérêts
Conflict of interest The authors declared no conflict of interest for this review.