Evidence map›Paper›PMID 35920669›Full record

ArticleMolecular and cellular biology2022

The Conserved CNOT1 Interaction Motif of Tristetraprolin Regulates ARE-mRNA Decay Independently of the p38 MAPK-MK2 Kinase Pathway.

Alberto Carreño, Jens Lykke-Andersen

Open access · hybridAbstract read
In one paragraph

Article in Molecular and cellular biology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
1.0field-weighted citation impact, top 25% 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

10 citing papers in PubMed, 13 citations in OpenAlex.

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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

2 authors at 1 institution in 1 country.

Alberto CarreñoDepartment of Molecular Biology, School of Biological Sciences, University of California San Diego, La Jolla, California, USA.
Jens Lykke-AndersenDepartment of Molecular Biology, School of Biological Sciences, University of California San Diego, La Jolla, California, USA.ORCID 0000-0003-1821-0754
University of California San Diego · US

Funding

Mechanisms of human RNA turnover and quality controlR35GM118069 · NIGMS · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI LYKKE-ANDERSEN, JENS · 2016 to 2025
$5.1M
Regulation of Tristetraprolin-mediated mRNA decay by signaling pathways in the inflammatory responseF31GM128320 · NIGMS · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI CARRENO, ALBERTO · 2019 to 2021
$115k
NIGMS NIH HHS F31 GM128320NIGMS NIH HHS R35 GM118069
6 · The paper itself

Abstract

The regulation of the mRNA decay activator Tristetraprolin (TTP) by the p38 mitogen-activated protein kinase (MAPK) pathway during the mammalian inflammatory response represents a paradigm for the control of mRNA turnover by signaling. TTP activity is regulated through multiple phosphorylation sites, including an evolutionary conserved serine in its CNOT1 Interacting Motif (CIM) whose phosphorylation disrupts an interaction with CNOT1 of the CCR4-NOT deadenylase complex. Here we present evidence that the TTP CIM recruits the CCR4-NOT deadenylase complex and activates mRNA degradation cooperatively with the conserved tryptophan residues of TTP, previously identified to interact with CNOT9. Surprisingly, the TTP CIM remains unphosphorylated and capable of promoting association with the CCR4-NOT complex and mRNA decay upon activation of p38-MAPK-activated kinase MK2, a well-established regulator of TTP activity. The CIM is instead targeted by other kinases including PKCα. These observations suggest that signaling pathways regulate TTP activity in a cooperative manner and that the p38 MAPK-MK2 kinase pathway relies on the activation of additional kinase pathway(s) to fully control TTP function.

Indexed as

Mitogen-Activated Protein Kinase 14TristetraprolinAnimalsIntracellular Signaling Peptides and ProteinsMammalsMitogen-Activated Protein Kinase Kinasesp38 Mitogen-Activated Protein KinasesPhosphorylationProtein Kinase C-alphaProtein Serine-Threonine KinasesRNA, MessengerRNA StabilitySerineTryptophanIntracellular Signaling Peptides and ProteinsMitogen-Activated Protein Kinase 14Mitogen-Activated Protein Kinase Kinasesp38 Mitogen-Activated Protein KinasesProtein Kinase C-alphaProtein Serine-Threonine KinasesRNA, MessengerSerineTristetraprolinTryptophanmRNA degradationmRNA stabilityposttranscriptional RNA-binding proteinsprotein phosphorylationTristetraprolin

Identifiers

PMID35920669
PMCPMC9476947
OpenAlexW4289550063

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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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.