Gene Symbol: Tbc1d4
Description: TBC1 domain family, member 4
Alias: RGD1561609, LOW QUALITY PROTEIN: TBC1 domain family member 4, TBC1 domain family member 4
Species: rat
Products:     Tbc1d4

Top Publications

  1. Dash S, Sano H, Rochford J, Semple R, Yeo G, Hyden C, et al. A truncation mutation in TBC1D4 in a family with acanthosis nigricans and postprandial hyperinsulinemia. Proc Natl Acad Sci U S A. 2009;106:9350-5 pubmed publisher
    Tre-2, BUB2, CDC16, 1 domain family member 4 (TBC1D4) (AS160) is a Rab-GTPase activating protein implicated in insulin-stimulated glucose transporter 4 (GLUT4) translocation in adipocytes and myotubes...
  2. Larance M, Ramm G, James D. The GLUT4 code. Mol Endocrinol. 2008;22:226-33 pubmed
    ..Many are now taking on this challenge. ..
  3. Kaddai V, Le Marchand Brustel Y, Cormont M. Rab proteins in endocytosis and Glut4 trafficking. Acta Physiol (Oxf). 2008;192:75-88 pubmed publisher
  4. Zaid H, Antonescu C, Randhawa V, Klip A. Insulin action on glucose transporters through molecular switches, tracks and tethers. Biochem J. 2008;413:201-15 pubmed publisher
  5. Alkhateeb H, Chabowski A, Glatz J, Gurd B, Luiken J, Bonen A. Restoring AS160 phosphorylation rescues skeletal muscle insulin resistance and fatty acid oxidation while not reducing intramuscular lipids. Am J Physiol Endocrinol Metab. 2009;297:E1056-66 pubmed publisher
  6. Fang P, Yu M, He B, Guo L, Huang X, Kong G, et al. Central injection of GALR1 agonist M617 attenuates diabetic rat skeletal muscle insulin resistance through the Akt/AS160/GLUT4 pathway. Mech Ageing Dev. 2017;162:122-128 pubmed publisher
    ..In conclusion, central injection of M617 mitigated insulin resistance of skeletal muscle by enhancing GLUT4 translocation from intracellular pools to plasma membranes via the activation of the Akt/AS160/GLUT4 signaling pathway. ..
  7. Mikłosz A, Łukaszuk B, Zendzian Piotrowska M, Branska Januszewska J, Ostrowska H, Chabowski A. Challenging of AS160/TBC1D4 Alters Intracellular Lipid milieu in L6 Myotubes Incubated With Palmitate. J Cell Physiol. 2017;232:2373-2386 pubmed publisher
    ..J. Cell. Physiol. 232: 2373-2386, 2017. © 2016 The Authors. Journal of Cellular Physiology Published by Wiley Periodicals Inc. ..
  8. Ishikura S, Klip A. Muscle cells engage Rab8A and myosin Vb in insulin-dependent GLUT4 translocation. Am J Physiol Cell Physiol. 2008;295:C1016-25 pubmed publisher
    ..These results support a model whereby AS160, Rab8A, and myosin Vb are required for insulin-induced GLUT4 translocation in muscle cells, potentially as part of a linear signaling cascade. ..
  9. Koumanov F, Richardson J, Murrow B, Holman G. AS160 phosphotyrosine-binding domain constructs inhibit insulin-stimulated GLUT4 vesicle fusion with the plasma membrane. J Biol Chem. 2011;286:16574-82 pubmed publisher
    AS160 (TBC1D4) is a known Akt substrate that is phosphorylated downstream of insulin action and that leads to regulated traffic of GLUT4...

More Information


  1. Chen Y, Wang Y, Zhang J, Deng Y, Jiang L, Song E, et al. Rab10 and myosin-Va mediate insulin-stimulated GLUT4 storage vesicle translocation in adipocytes. J Cell Biol. 2012;198:545-60 pubmed publisher
    ..Thus, multiple Rab proteins regulate the trafficking of GLUT4, with Rab10 coordinating with myosin-Va to mediate the final steps of insulin-stimulated GSV translocation to the PM...
  2. Sharma N, Arias E, Cartee G. Rapid reversal of insulin-stimulated AS160 phosphorylation in rat skeletal muscle after insulin exposure. Physiol Res. 2010;59:71-8 pubmed
  3. Funai K, Schweitzer G, Sharma N, Kanzaki M, Cartee G. Increased AS160 phosphorylation, but not TBC1D1 phosphorylation, with increased postexercise insulin sensitivity in rat skeletal muscle. Am J Physiol Endocrinol Metab. 2009;297:E242-51 pubmed publisher
    ..They also support the idea that increased TBC1D1 phosphorylation may play a role in the insulin-independent increase in GT postexercise. ..
  4. Kawamoto E, Koshinaka K, Yoshimura T, Masuda H, Kawanaka K. Immobilization rapidly induces muscle insulin resistance together with the activation of MAPKs (JNK and p38) and impairment of AS160 phosphorylation. Physiol Rep. 2016;4: pubmed publisher
    ..Elevated ceramide biosynthesis pathway may contribute to this activation. Our results also indicate that decreased basal phosphorylation of AS160 may be involved in inactivity-induced insulin resistance. ..
  5. Watson R, Pessin J. GLUT4 translocation: the last 200 nanometers. Cell Signal. 2007;19:2209-17 pubmed
    ..Future work will focus on identifying the key insulin targets that regulate the GLUT4 docking/fusion processes. ..