ArticleBiochemical and biophysical research communications2009
Developmentally spliced PKCbetaII provides a possible link between mTORC2 and Akt kinase to regulate 3T3-L1 adipocyte insulin-stimulated glucose transport.
Article in Biochemical and biophysical research communications, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 29 citations in OpenAlex.
- Selective chemical and genetic inhibition of PKCβII strongly sensitizes colon cancer cells to anoikis.Molecular biology reports · 2025Article
- Lysozyme Gene Expression in 3T3-L1 Cells Sustains Expression of Adipogenic Genes and Adipocyte Differentiation.Frontiers in cell and developmental biology · 2022Article
- Regulatory roles and mechanisms of alternative RNA splicing in adipogenesis and human metabolic health.Cell & bioscience · 2021Review
- Identification of Sortilin Alternatively Spliced Variants in Mouse 3T3L1 Adipocytes.International journal of molecular sciences · 2021Article
- Stabilization of lncRNA GAS5 by a Small Molecule and Its Implications in Diabetic Adipocytes.Cell chemical biology · 2019Article
- Egg white hydrolysate shows insulin mimetic and sensitizing effects in 3T3-F442A pre-adipocytes.PloS one · 2017Article
- Emerging role of protein kinase C in energy homeostasis: A brief overview.World journal of diabetes · 2014Review
- Clk/STY (cdc2-like kinase 1) and Akt regulate alternative splicing and adipogenesis in 3T3-L1 pre-adipocytes.PloS one · 2013Article
- Real-Time Translocation and Function of PKCβII Isoform in Response to Nociceptive Signaling via the TRPV1 Pain Receptor.Pharmaceuticals (Basel, Switzerland) · 2011Article
- Mechanical regulation of glycogen synthase kinase 3β (GSK3β) in mesenchymal stem cells is dependent on Akt protein serine 473 phosphorylation via mTORC2 protein.The Journal of biological chemistry · 2011Article
- Oxidative stress and the etiology of insulin resistance and type 2 diabetes.Free radical biology & medicine · 2011Review
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
Functional adipocyte glucose disposal is a key component of global glucose homeostasis. PKCbetaII is involved in rat skeletal muscle cell ISGT. Western blot analysis and real-time PCR revealed 3T3-L1 cells developmentally regulated PKCbeta splicing such that PKCbetaI was downregulated and PKCbetaII was upregulated during the course of differentiation. An initial glucose uptake screen using PKC inhibitor LY379196 pointed to a PKC isozyme other than PKCzeta mediating 3T3-L1 adipocyte ISGT. Subsequent use of PKCbetaII inhibitor CGP53353 pointed to a role for PKCbetaII in ISGT. Western blot analysis showed that CGP53353 specifically inhibited phosphorylation of PKCbetaII Serine 660. Subcellular fractionation and immunofluorescence demonstrated that PKCbetaII regulates GLUT4 translocation. Further Western blot, immunofluorescence and co-immunoprecipitation analysis reveal that PKCbetaII inhibition does not affect mTORC2 activity yet abrogates phosphorylation of Akt Serine 473. PKCbetaII regulates GLUT4 translocation by regulating Akt phosphorylation and thus activity.
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