ArticleBMC molecular biology2006
Functional characterisation of the regulation of CAAT enhancer binding protein alpha by GSK-3 phosphorylation of Threonines 222/226.
Article in BMC molecular biology, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 28 citations in OpenAlex.
- Review
- Glycogen synthase kinase (GSK)-3 and the double-strand RNA-dependent kinase, PKR: When two kinases for the common good turn bad.Biochimica et biophysica acta. Molecular cell research · 2020Review
- Review
- Inhibition of Casein Kinase 2 Disrupts Differentiation of Myeloid Cells in Cancer and Enhances the Efficacy of Immunotherapy in Mice.Cancer research · 2018Article
- Ndrg1 promotes adipocyte differentiation and sustains their function.Scientific reports · 2017Article
- Triptolide in the treatment of psoriasis and other immune-mediated inflammatory diseases.British journal of clinical pharmacology · 2012Review
- Identification of a proline-rich inositol polyphosphate 5-phosphatase (PIPP)•collapsin response mediator protein 2 (CRMP2) complex that regulates neurite elongation.The Journal of biological chemistry · 2011Article
- CCAAT/enhancer-binding protein alpha (C/EBPalpha) is critical for interleukin-4 expression in response to FcepsilonRI receptor cross-linking.The Journal of biological chemistry · 2011Article
- What Are the bona fide GSK3 Substrates?International journal of Alzheimer's disease · 2011Article
- GSK-3: Functional Insights from Cell Biology and Animal Models.Frontiers in molecular neuroscience · 2011Article
- The ubiquitin ligase Fbxw7 controls adipocyte differentiation by targeting C/EBPalpha for degradation.Proceedings of the National Academy of Sciences of the United States of America · 2010Article
- Triptolide inhibits IL-12/IL-23 expression in APCs via CCAAT/enhancer-binding protein alpha.Journal of immunology (Baltimore, Md. : 1950) · 2010Article
- The nucleocapsid protein of SARS-CoV induces transcription of hfgl2 prothrombinase gene dependent on C/EBP alpha.Journal of biochemistry · 2008Article
- Phosphorylation of CCAAT/enhancer-binding protein alpha regulates GLUT4 expression and glucose transport in adipocytes.The Journal of biological chemistry · 2008Article
- Kaposi's sarcoma-associated herpesvirus LANA protein downregulates nuclear glycogen synthase kinase 3 activity and consequently blocks differentiation.Journal of virology · 2007Article
- Immunosuppressive, anti-inflammatory and anti-cancer properties of triptolide: A mini review.Avicenna journal of phytomedicineReview
- Sumoylation and the function of CCAAT enhancer binding protein alpha (C/EBP alpha).Blood cells, molecules & diseasesReview
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundGlycogen Synthase Kinase-3 (GSK3) activity is repressed following insulin treatment of cells. Pharmacological inhibition of GSK3 mimics the effect of insulin on Phosphoenolpyruvate Carboxykinase (PEPCK), Glucose-6 Phosphatase (G6Pase) and IGF binding protein-1 (IGFBP1) gene expression. CAAT/enhancer binding protein alpha (C/EBPalpha) regulates these gene promoters in liver and is phosphorylated on two residues (T222/T226) by GSK3, although the functional outcome of the phosphorylation has not been established. We aimed to establish whether CEBPalpha is a link between GSK3 and these gene promoters.
resultsC/EBPalpha represses the IGFBP1 thymine-rich insulin response element (TIRE), but mutation of T222 or T226 of C/EBPalpha to non-phosphorylatable alanines has no effect on C/EBPalpha activity in liver cells (towards the TIRE or a consensus C/EBP binding sequence). Phosphorylation of T222/T226 is decreased by GSK3 inhibition, suggesting GSK3 does phosphorylate T222/226 in intact cells. However, phosphorylation was not altered by treatment of liver cells with insulin. Meanwhile C/EBPalpha activity in 3T3 L1 preadipocytes was enhanced by mutation of T222/T226 and/or S230 to alanine residues. Finally, we demonstrate that C/EBPalpha is a very poor substrate for GSK3 in vitro and in cells.
conclusionThe work demonstrates an important role for this domain in the regulation of C/EBPalpha activity in adipocytes but not hepatocytes, however GSK3 phosphorylation of these residues does not mediate regulation of this C/EBP activity. In short, we find no evidence that C/EBPalpha activity is regulated by direct phosphorylation by GSK3.
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