Evidence map›Paper›PMID 35129087›Full record

ArticleRNA biology2022

Regulation of CCR4-NOT complex deadenylase activity and cellular responses by MK2-dependent phosphorylation of CNOT2.

Toru Suzuki, Miyuki Hoshina, Saori Nishijima, Naosuke Hoshina, Chisato Kikuguchi, Takumi Tomohiro, Akira Fukao, Toshinobu Fujiwara, Tadashi Yamamoto

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in RNA biology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
0.3field-weighted citation impact, top 50% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

2 citing papers in PubMed, 3 citations in OpenAlex.

  1. Article
  2. Elucidating the Role ofCurrent issues in molecular biology · 2025
    Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

9 authors at 3 institutions in 1 country.

Toru SuzukiLaboratory for Immunogenetics, Center for Integrative Medical Sciences, Riken, Yokohama, Japan.ORCID 0000-0003-1864-8027
Miyuki HoshinaCell Signal Unit, Okinawa Institute of Science and Technology Graduate University, Onna, Japan.
Saori NishijimaCell Signal Unit, Okinawa Institute of Science and Technology Graduate University, Onna, Japan.
Naosuke HoshinaCell Signal Unit, Okinawa Institute of Science and Technology Graduate University, Onna, Japan.
Chisato KikuguchiLaboratory for Immunogenetics, Center for Integrative Medical Sciences, Riken, Yokohama, Japan.
Takumi TomohiroLaboratory of Biochemistry, Kindai University, Higashi-Osaka, Japan.
Akira FukaoLaboratory of Biochemistry, Kindai University, Higashi-Osaka, Japan.
Toshinobu FujiwaraLaboratory of Biochemistry, Kindai University, Higashi-Osaka, Japan.
Tadashi YamamotoCell Signal Unit, Okinawa Institute of Science and Technology Graduate University, Onna, Japan.ORCID 0000-0002-5938-9378
Okinawa Institute of Science and Technology Graduate University · JPKindai University · JPRIKEN Center for Integrative Medical Sciences · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

CCR4-NOT complex-mediated mRNA deadenylation serves critical functions in multiple biological processes, yet how this activity is regulated is not fully understood. Here, we show that osmotic stress induces MAPKAPK-2 (MK2)-mediated phosphorylation of CNOT2. Programmed cell death is greatly enhanced by osmotic stress in CNOT2-depleted cells, indicating that CNOT2 is responsible for stress resistance of cells. Although wild-type (WT) and non-phosphorylatable CNOT2 mutants reverse this sensitivity, a phosphomimetic form of CNOT2, in which serine at the phosphorylation site is replaced with glutamate, does not have this function. We also show that mRNAs have elongated poly(A) tails in CNOT2-depleted cells and that introduction of CNOT2 WT or a non-phosphorylatable mutant, but not phosphomimetic CNOT2, renders their poly(A) tail lengths comparable to those in control HeLa cells. Consistent with this, the CCR4-NOT complex containing phosphomimetic CNOT2 exhibits less deadenylase activity than that containing CNOT2 WT. These data suggest that CCR4-NOT complex deadenylase activity is regulated by post-translational modification, yielding dynamic control of mRNA deadenylation.

Indexed as

Cell LineEnzyme ActivationHumansIntracellular Signaling Peptides and ProteinsMAP-Kinase-Activated Kinase 2Multiprotein ComplexesNuclear Receptor Subfamily 4, Group A, Member 2Osmotic PressurePhosphorylationProtein Serine-Threonine KinasesReceptors, CCR4Repressor ProteinsRNA, MessengerRNA StabilityStress, PhysiologicalCCR4 protein, humanCNOT2 protein, humanIntracellular Signaling Peptides and ProteinsMAP-Kinase-Activated Kinase 2Multiprotein ComplexesNR4A2 protein, humanNuclear Receptor Subfamily 4, Group A, Member 2Protein Serine-Threonine KinasesReceptors, CCR4Repressor ProteinsRNA, MessengerCCR4-NOT complexMK2mRNA decayphosphorylationstress response

Identifiers

PMID35129087
PMCPMC8820811
OpenAlexW4213063931

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.