ArticleThe Journal of biological chemistry2008
Phosphorylation of CCAAT/enhancer-binding protein alpha regulates GLUT4 expression and glucose transport in adipocytes.
Article in The Journal of biological chemistry, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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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.
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Who cites it
15 citing papers in PubMed, 22 citations in OpenAlex.
- A novel C/EBPα-miR-335-5p-PRKAA2 regulatory axis drives hepatic lipid accumulation in MASLD.Scientific reports · 2026Article
- C/EBPα plays a critical role in adipocyte differentiation and obesity.Frontiers in molecular biosciences · 2026Review
- Role of Non-Coding RNAs in White and Brown Adipose Tissue Differentiation and Development.Non-coding RNA · 2025Review
- Excessive or sustained endoplasmic reticulum stress: one of the culprits of adipocyte dysfunction in obesity.Therapeutic advances in endocrinology and metabolism · 2024Review
- Activating transcription factor 3 coordinates differentiation of cardiac and hematopoietic progenitors by regulating glucose metabolism.Science advances · 2020Article
- Dlk1 expression relates to visceral fat expansion and insulin resistance in male and female rats with postnatal catch-up growth.Pediatric research · 2019Article
- Conjugated Linoleic Acid Supplementation Improves Maternal High Fat Diet-Induced Programming of Metabolic Dysfunction in Adult Male Rat Offspring.Scientific reports · 2017Article
- PI3K-resistant GSK3 controls adiponectin formation and protects from metabolic syndrome.Proceedings of the National Academy of Sciences of the United States of America · 2016Article
- Lipopolysaccharide binding protein is an adipokine involved in the resilience of the mouse adipocyte to inflammation.Diabetologia · 2015Article
- A novel crosstalk between TLR4- and NOD2-mediated signaling in the regulation of intestinal inflammation.Scientific reports · 2015Article
- Targeting CDK1 promotes FLT3-activated acute myeloid leukemia differentiation through C/EBPα.The Journal of clinical investigation · 2012Article
- 12/15-Lipoxygenase signaling in the endoplasmic reticulum stress response.American journal of physiology. Endocrinology and metabolism · 2012Article
- Triptolide inhibits IL-12/IL-23 expression in APCs via CCAAT/enhancer-binding protein alpha.Journal of immunology (Baltimore, Md. : 1950) · 2010Article
- C/EBPalpha and the corepressors CtBP1 and CtBP2 regulate repression of select visceral white adipose genes during induction of the brown phenotype in white adipocytes by peroxisome proliferator-activated receptor gamma agonists.Molecular and cellular biology · 2009Article
- Regulation of cyclin D1 and Wnt10b gene expression by cAMP-responsive element-binding protein during early adipogenesis involves differential promoter methylation.The Journal of biological chemistry · 2008Article
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
Abstract
The transcription factor CCAAT/enhancer-binding protein alpha (C/EBPalpha) is required during adipogenesis for development of insulin-stimulated glucose uptake. Modes for regulating this function of C/EBPalpha have yet to be determined. Phosphorylation of C/EBPalpha on Ser-21 has been implicated in the regulation of granulopoiesis and hepatic gene expression. To explore the role of Ser-21 phosphorylation on C/EBPalpha function during adipogenesis, we developed constructs in which Ser-21 was mutated to alanine (S21A) to model dephosphorylation. In two cell culture models deficient in endogenous C/EBPalpha, enforced expression of S21A-C/EBPalpha resulted in normal lipid accumulation and expression of many adipogenic markers. However, S21A-C/EBPalpha had impaired ability to activate the Glut4 promoter specifically, and S21A-C/EBPalpha expression resulted in diminished GLUT4 and adiponectin expression, as well as reduced insulin-stimulated glucose uptake. No defects in insulin signaling or GLUT4 vesicle trafficking were identified with S21A-C/EBPalpha expression, and when exogenous GLUT4 expression was enforced to normalize expression in S21A-C/EBPalpha cells, insulin-responsive glucose transport was reconstituted, suggesting that the primary defect was a deficit in GLUT4 levels. Mice in which endogenous C/EBPalpha was replaced with S21A-C/EBPalpha displayed reduced GLUT4 and adiponectin protein expression in epididymal adipose tissue and increased blood glucose compared with wild-type littermates. These results suggest that phosphorylation of C/EBPalpha on Ser-21 may regulate adipocyte gene expression and whole body glucose homeostasis.
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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.