Tctex1d2 Is a Negative Regulator of GLUT4 Translocation and Glucose Uptake

DOI PDF PubMed 参考文献19件
  • Yoko Shimoda
    Department of Medicine and Molecular Science (Y.S., S.O., E.Y., M.Y.), Gunma University Graduate School of Medicine, Gunma 371-8511, Japan
  • Shuichi Okada
    Department of Medicine and Molecular Science (Y.S., S.O., E.Y., M.Y.), Gunma University Graduate School of Medicine, Gunma 371-8511, Japan
  • Eijiro Yamada
    Department of Medicine and Molecular Science (Y.S., S.O., E.Y., M.Y.), Gunma University Graduate School of Medicine, Gunma 371-8511, Japan
  • Jeffrey E. Pessin
    Departments of Medicine and Molecular Pharmacology (J.E.P.), Albert Einstein College of Medicine, Bronx, New York 10461
  • Masanobu Yamada
    Department of Medicine and Molecular Science (Y.S., S.O., E.Y., M.Y.), Gunma University Graduate School of Medicine, Gunma 371-8511, Japan

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説明

Tctex1d2 (Tctex1 domain containing 2) is an open reading frame that encodes for a functionally unknown protein that contains a Tctex1 domain found in dynein light chain family members. Examination of gene expression during adipogenesis demonstrated a marked increase in Tctex1d2 protein expression that was essentially undetectable in preadipocytes and markedly induced during 3T3-L1 adipocyte differentiation. Tctex1d2 overexpression significantly inhibited insulin-stimulated glucose transporter 4 (GLUT4) translocation and 2-deoxyglucose uptake. In contrast, Tctex1d2 knockdown significantly increased insulin-stimulated GLUT4 translocation and 2-deoxyglucose uptake. However, acute insulin stimulation (up to 30 min) in 3T3-L1 adipocytes with overexpression or knockdown of Tctex1d2 had no effect on Akt phosphorylation, a critical signal transduction target required for GLUT4 translocation. Although overexpression of Tctex1d2 had no significant effect on GLUT4 internalization, Tctex1d2 was found to associate with syntaxin 4 in an insulin-dependent manner and inhibit Doc2b binding to syntaxin 4. In addition, glucose-dependent insulinotropic polypeptide rescued the Tctex1d2 inhibition of insulin-stimulated GLUT4 translocation by suppressing the Tctex1d2-syntaxin 4 interaction and increasing Doc2b-Synatxin4 interactions. Taking these results together, we hypothesized that Tctex1d2 is a novel syntaxin 4 binding protein that functions as a negative regulator of GLUT4 plasma membrane translocation through inhibition of the Doc2b-syntaxin 4 interaction.

収録刊行物

  • Endocrinology

    Endocrinology 156 (10), 3548-3558, 2015-07-22

    The Endocrine Society

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