ArticleJournal of cellular physiology2016
Mitogen-Dependent Regulation of DUSP1 Governs ERK and p38 Signaling During Early 3T3-L1 Adipocyte Differentiation.
Article in Journal of cellular physiology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 32 citations in OpenAlex.
- Interplay between miR27a and PPARγ-DUSP1 regulates BPXV mRNA translation via modulating p38α MAPK-MNK1-eIF4E signaling pathway.Virus research · 2026Article
- Transient activation of ciliary CCR2 signaling promotes the initiation of adipogenesis.Nature communications · 2026Article
- SLFN11 enhances cisplatin sensitivity in pediatric cancer via activation of stress-response and suppression of survival pathways.British journal of cancer · 2026Article
- Ribosome-associated quality control of aberrant protein production during amino acid limitation.bioRxiv : the preprint server for biology · 2026Article
- Hepatic protein kinase Cβ antagonizing p38American journal of physiology. Gastrointestinal and liver physiology · 2025Article
- Inactivation of CDK4/6, CDK2, and ERK in G1-phase triggers differentiation commitment.Communications biology · 2025Article
- Article
- MiR-26a Inhibits Porcine Adipogenesis by Regulating ACADM and ACSL1 Genes and Cell Cycle Progression.Animals : an open access journal from MDPI · 2024Article
- Article
- Computational evidence for multi-layer crosstalk between the cadherin-11 and PDGFR pathways.Scientific reports · 2023Article
- ING4 Promotes Stemness Enrichment of Human Renal Cell Carcinoma Cells Through Inhibiting DUSP4 Expression to Activate the p38 MAPK/type I IFN-Stimulated Gene Signaling Pathway.Frontiers in pharmacology · 2022Article
- Article
- Article
- Myostatin suppresses adipogenic differentiation and lipid accumulation by activating crosstalk between ERK1/2 and PKA signaling pathways in porcine subcutaneous preadipocytes.Journal of animal science · 2021Article
- Review
- SINO Syndrome Causative KIDINS220/ARMS Gene Regulates Adipocyte Differentiation.Frontiers in cell and developmental biology · 2021Article
- Expression Profiling of the MAP Kinase Phosphatase Family Reveals a Role for DUSP1 in the Glioblastoma Stem Cell Niche.Cancer microenvironment : official journal of the International Cancer Microenvironment Society · 2017Article
- Sex Steroid Hormones Regulate Leptin Transcript Accumulation and Protein Secretion in 3T3-L1 Cells.Scientific reports · 2017Article
- Obesity Modulates Inflammation and Lipid Metabolism Oocyte Gene Expression: A Single-Cell Transcriptome Perspective.The Journal of clinical endocrinology and metabolism · 2017Article
- pERK-dependent defective TCR-mediated activation of CD4Immunity & ageing : I & A · 2017Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
Knowledge concerning mechanisms that control proliferation and differentiation of preadipocytes is essential to our understanding of adipocyte hyperplasia and the development of obesity. Evidence has shown that temporal regulation of mitogen-activated protein kinase (MAPK) phosphorylation and dephosphorylation is critical for coupling extracellular stimuli to cellular growth and differentiation. Using differentiating 3T3-L1 preadipocytes as a model of adipocyte hyperplasia, we examined a role for dual-specificity phosphatase 1 (DUSP1) on the timely modulation of MAPK signaling during states of growth arrest, proliferation, and differentiation. Using real-time reverse transcription PCR (qRT-PCR), we report that DUSP1 is induced during early preadipocyte proliferation concomitant with ERK and p38 dephosphorylation. As deactivation of ERK and p38 is essential for the progression of adipocyte differentiation, we further showed that de novo mRNA synthesis was required for ERK and p38 dephosphorylation, suggesting a role for "inducible" phosphatases in regulating MAPK signaling. Pharmacological and genetic inhibition of DUSP1 markedly increased ERK and p38 phosphorylation during early adipocyte differentiation. Based on these findings, we postulated that loss of DUSP1 would block adipocyte hyperplasia. However, genetic loss of DUSP1 was not sufficient to prevent preadipocyte proliferation or differentiation, suggesting a role for other phosphatases in the regulation of adipogenesis. In support of this, qRT-PCR identified several MAPK-specific DUSPs induced during early (DUSP2, -4, -5, & -6), mid (DUSP4 & -16) and late (DUSP9) stages of adipocyte differentiation. Collectively, these data suggest an important role for DUSPs in regulating MAPK dephosphorylation, with an emphasis on DUSP1, during early adipogenesis.
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Registered trials
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.