Results 11 to 20 of about 14,275 (206)

Rapid nuclear deadenylation of mammalian messenger RNA [PDF]

open access: yesiScience, 2023
Summary: Poly(A) tails protect RNAs from degradation and their deadenylation rates determine RNA stability. Although poly(A) tails are generated in the nucleus, deadenylation of tails has mostly been investigated within the cytoplasm.
Jonathan Alles   +3 more
doaj   +5 more sources

Reconstitution of recombinant human CCR4-NOT reveals molecular insights into regulated deadenylation

open access: yesNature Communications, 2019
The CCR4-NOT complex shortens poly(A) tails of messenger RNAs. By biochemical reconstitution of the entire human CCR4-NOT complex, the authors show the stimulatory roles of non-enzymatic subunits and the importance of the interaction between CAF40 and ...
Tobias Raisch   +2 more
exaly   +2 more sources

MARTRE family proteins negatively regulate CCR4-NOT activity to protect poly(A) tail length and promote translation of maternal mRNA [PDF]

open access: yesNature Communications
The mammalian early embryo development requires translation of maternal mRNA inherited from the oocyte. While poly(A) tail length influences mRNA translation efficiency during the oocyte-to-embryo transition (OET), molecular mechanisms regulating ...
Jing Yang   +8 more
doaj   +2 more sources

An extended wave of global mRNA deadenylation sets up a switch in translation regulation across the mammalian oocyte-to-embryo transition

open access: yesCell Reports
Summary: Without new transcription, gene expression across the oocyte-to-embryo transition (OET) relies instead on regulation of mRNA poly(A) tails to control translation.
Heidi Cook-Andersen, Robert Morey
exaly   +3 more sources

Stoichiometry and Change of the mRNA Closed-Loop Factors as Translating Ribosomes Transit from Initiation to Elongation [PDF]

open access: yes, 2016
Protein synthesis is a highly efficient process and is under exacting control. Yet, the actual abundance of translation factors present in translating complexes and how these abundances change during the transit of a ribosome across an mRNA remains ...
Chiang, Yueh-Chin   +6 more
core   +15 more sources

microRNA-mediated messenger RNA deadenylation contributes to translational repression in mammalian cells. [PDF]

open access: yesPLoS ONE, 2009
Animal microRNAs (miRNAs) typically regulate gene expression by binding to partially complementary target sites in the 3' untranslated region (UTR) of messenger RNA (mRNA) reducing its translation and stability.
Traude H Beilharz   +6 more
doaj   +1 more source

RNF219 RING Finger Domain Mutants Drive Phase Separation to Encapsulate CCR4-NOT and Promote Cell Proliferation. [PDF]

open access: yesCell Prolif
Mutations in the RING finger domain (C3HC4) of RNF219 promote the formation of RNF219 condensates, which are able to encapsulate the CCR4‐NOT complex. These RNF219Mut‐CCR4‐NOT condensates reduce the deacetylation activity of the CCR4‐NOT complex and induce cell proliferation.
Chen C, Guo C, Fang K, Lin C, Luo Z.
europepmc   +2 more sources

mRNA deadenylation by Pan2–Pan3 [PDF]

open access: yesBiochemical Society Transactions, 2014
Poly(A) tails are important regulators of mRNA stability and translational efficiency. Cytoplasmic removal of poly(A) tails by 3′→5′ exonucleases (deadenylation) is the rate-limiting step in mRNA degradation. Two exonuclease complexes contribute the majority of the deadenylation activity in eukaryotes: Ccr4–Not and Pan2–Pan3.
Wolf J, Passmore LA.
openaire   +2 more sources

Interaction between NANOS2 and the CCR4-NOT deadenylation complex is essential for male germ cell development in mouse. [PDF]

open access: yesPLoS ONE, 2012
Nanos is one of the evolutionarily conserved proteins implicated in germ cell development and we have previously shown that it interacts with the CCR4-NOT deadenylation complex leading to the suppression of specific RNAs. However, the molecular mechanism
Atsushi Suzuki   +4 more
doaj   +1 more source

mRNA deadenylation and telomere disease [PDF]

open access: yesJournal of Clinical Investigation, 2015
Dyskeratosis congenita (DC) is an inherited BM failure disorder that is associated with mutations in genes involved with telomere function and maintenance; however, the genetic cause of many instances of DC remains uncharacterized. In this issue of the JCI, Tummala and colleagues identify mutations in the gene encoding the poly(A)-specific ribonuclease
Philip J, Mason, Monica, Bessler
openaire   +3 more sources

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