Evidence map›Paper›PMID 37086408›Full record

ArticleCell reports2023

ZFP36-mediated mRNA decay regulates metabolism.

Andrew C Cicchetto, Elsie C Jacobson, Hannah Sunshine, Blake R Wilde, Abigail S Krall, Kelsey E Jarrett, Leslie Sedgeman, Martin Turner, Kathrin Plath, M Luisa Iruela-Arispe and 2 more

Open access · goldAbstract read
In one paragraph

Article in Cell reports, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
5.5field-weighted citation impact, top 4% 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

30 citing papers in PubMed, 36 citations in OpenAlex.

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  18. Dietary Fermentation withInternational journal of molecular sciences · 2025
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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

12 authors at 3 institutions in 2 countries.

Andrew C CicchettoDepartment of Biological Chemistry, University of California, Los Angeles (UCLA), Los Angeles, CA, USA.
Elsie C JacobsonDepartment of Biological Chemistry, University of California, Los Angeles (UCLA), Los Angeles, CA, USA.
Hannah SunshineDepartment of Cell and Developmental Biology, Feinberg School of Medicine, Northwestern University, Chicago, IL, USA.
Blake R WildeDepartment of Biological Chemistry, University of California, Los Angeles (UCLA), Los Angeles, CA, USA.
Abigail S KrallDepartment of Biological Chemistry, University of California, Los Angeles (UCLA), Los Angeles, CA, USA.
Kelsey E JarrettDepartment of Biological Chemistry, University of California, Los Angeles (UCLA), Los Angeles, CA, USA; Department of Medicine, Division of Cardiology, UCLA, Los Angeles, CA, USA.
Leslie SedgemanDepartment of Biological Chemistry, University of California, Los Angeles (UCLA), Los Angeles, CA, USA; Department of Medicine, Division of Cardiology, UCLA, Los Angeles, CA, USA.
Martin TurnerImmunology Programme, The Babraham Institute, Cambridge, UK.
Kathrin PlathDepartment of Biological Chemistry, University of California, Los Angeles (UCLA), Los Angeles, CA, USA; Eli and Edythe Broad Center of Regenerative Medicine and Stem Cell Research, UCLA, Los Angeles, CA, USA; Jonsson Comprehensive Cancer Center, UCLA, Los Angeles, CA, USA.
M Luisa Iruela-ArispeDepartment of Cell and Developmental Biology, Feinberg School of Medicine, Northwestern University, Chicago, IL, USA.
Thomas Q de Aguiar VallimDepartment of Biological Chemistry, University of California, Los Angeles (UCLA), Los Angeles, CA, USA; Department of Medicine, Division of Cardiology, UCLA, Los Angeles, CA, USA; Molecular Biology Institute, UCLA, Los Angeles, CA, USA; Jonsson Comprehensive Cancer Center, UCLA, Los Angeles, CA, USA.
Heather R ChristofkDepartment of Biological Chemistry, University of California, Los Angeles (UCLA), Los Angeles, CA, USA; Eli and Edythe Broad Center of Regenerative Medicine and Stem Cell Research, UCLA, Los Angeles, CA, USA; Jonsson Comprehensive Cancer Center, UCLA, Los Angeles, CA, USA. Electronic address: hchristofk@mednet.ucla.edu.
University of California, Los Angeles · USNorthwestern University · USBabraham Institute · GB

Funding

Women's CancersP30CA016042 · NCI · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI DENNIS J SLAMON · 1985 to 2026
$134.5M
Vascular Biology Training GrantT32HL069766 · NHLBI · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI LUSIS, ALDONS JAKE · 2002 to 2022
$7.4M
Nutrient Regulation of Cancer Cell GrowthR01CA215185 · NCI · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI Heather Christofk · 2018 to 2026
$4.3M
Metabolic Control of Hair Follicle Stem Cell Homeostasis and TumorigenesisR01AR070245 · NIAMS · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI CHRISTOFK, HEATHER, LOWRY, WILLIAM E · 2018 to 2022
$2.1M
Metabolic Control of Hair Follicle Stem Cell Homeostasis and TumorigenesisR01AR084245 · NIAMS · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI Heather Christofk, William E Lowry · 2024 to 2026
$1.4M
NCI NIH HHS P30 CA016042NCI NIH HHS R01 CA215185NHLBI NIH HHS T32 HL069766NIAMS NIH HHS R01 AR070245NIAMS NIH HHS R01 AR084245
6 · The paper itself

Abstract

Cellular metabolism is tightly regulated by growth factor signaling, which promotes metabolic rewiring to support growth and proliferation. While growth factor-induced transcriptional and post-translational modes of metabolic regulation have been well defined, whether post-transcriptional mechanisms impacting mRNA stability regulate this process is less clear. Here, we present the ZFP36/L1/L2 family of RNA-binding proteins and mRNA decay factors as key drivers of metabolic regulation downstream of acute growth factor signaling. We quantitatively catalog metabolic enzyme and nutrient transporter mRNAs directly bound by ZFP36 following growth factor stimulation-many of which encode rate-limiting steps in metabolic pathways. Further, we show that ZFP36 directly promotes the mRNA decay of Enolase 2 (Eno2), altering Eno2 protein expression and enzymatic activity, and provide evidence of a ZFP36/Eno2 axis during VEGF-stimulated developmental retinal angiogenesis. Thus, ZFP36-mediated mRNA decay serves as an important mode of metabolic regulation downstream of growth factor signaling within dynamic cell and tissue states.

Indexed as

RNA-Binding ProteinsSignal TransductionIntercellular Signaling Peptides and ProteinsRNA StabilityTristetraprolinIntercellular Signaling Peptides and ProteinsRNA-Binding ProteinsTristetraprolinCP: MetabolismCP: Molecular biologygrowth factor signalingmetabolismmRNA stabilityRNA-binding proteins

Identifiers

PMID37086408
PMCPMC10332406
OpenAlexW4366607759

What OpenQuestion holds

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LicenceCC BY
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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.