Metabolism
How does ZFP36 reshape metabolism after growth signals?
Open access · cc by · source: Europe PMC
Growth factors induce ZFP36, which binds and decays metabolic enzyme/transporter mRNAs—especially Eno2—tuning glycolytic metabolism.
Study at a glance
- Design
- Animal / in-vitro — ZFP36 eCLIP, Eno2 decay, metabolomics, and endothelial Zfp36 loss in retinal angiogenesis
- N
- MEF and in-vivo angiogenesis assays — no single primary analytic N in stored text
- Population
- Mouse embryonic fibroblasts and neonatal retinal vasculature models
- Outcome
- ZFP36-mediated decay of metabolic mRNAs including Eno2
Structured fields used in claim comparison tables when every cited study has a complete layer.
Key findings
ZFP36 family members are acute growth-factor immediate-early genes; they bind many metabolic mRNAs and promote Eno2 mRNA decay; loss elevates ENO2/PEP and alters the metabolome; regulation appears in neonatal retinal angiogenesis.
Methodology
Mapped ZFP36 induction and eCLIP targets after growth-factor stimulation in MEFs, validated Eno2 decay, metabolomics, and retinal angiogenesis after endothelial Zfp36 loss.
Limitations
Does not prove Eno2 is the sole metabolic effector of ZFP36 in every tissue or that ZFP36 drugs would safely remodel metabolism clinically.
How this study connects
Role on claims
Each row is a claim on a concept or method page where this paper supports, challenges, or qualifies the statement. Roles are hand-checked — not a model guess.
Multiple empirical papers in this library examine metabolism with mechanistic biological findings.
Evidence for the claim as stated.
ZFP36 family members are acute growth-factor immediate-early genes; they bind many metabolic mRNAs and promote Eno2 mRNA decay; loss elevates ENO2/PEP and alters the metabolome; regulation appears in neonatal retinal angiogenesis.
Evidence for the claim as stated.
Systems and scales differ across metabolism studies (species, tissues, methods), so mechanisms should not be over-generalised.
Evidence for the claim as stated.
Two papers are weak luciferase examples. Foxp3 stability was scored by bisulphite sequencing and ChIP: a TSDR-like element is demethylated in stable Tregs, and weak demethylation predicts unstable TGF-β–induced Foxp3 (mostly mouse). ZFP36 family members are growth-factor immediate-early genes that bind metabolic mRNAs, promote Eno2 decay, raise ENO2/PEP when lost, and affect neonatal retinal angiogenesis — eCLIP and metabolomics, not a promoter-luciferase paper.
Evidence for the claim as stated.
MC4R shows that a cAMP/reporter signal can look normal while trafficking is impaired, so luciferase-like pathway readouts disagree with surface-expression assays. Foxp3 and ZFP36 papers barely use luciferase at all: DNA methylation/ChIP versus mRNA decay and metabolomics.
Evidence for the claim as stated.
Open questions
Tensions this paper is part of
From concept pages' “where studies disagree.” Disagreement means the same question; scope means different assays, populations, or outcomes.
Systems and scales differ across metabolism studies (species, tissues, methods), so mechanisms should not be over-generalised.
MC4R shows that a cAMP/reporter signal can look normal while trafficking is impaired, so luciferase-like pathway readouts disagree with surface-expression assays. Foxp3 and ZFP36 papers barely use luciferase at all: DNA methylation/ChIP versus mRNA decay and metabolomics.
- Supports · How MC4R variants scramble receptor trafficking
- Supports · Epigenetic locking of Foxp3 in Tregs
Related papers in this topic
Same topic cluster — not a recommendation engine.