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Supportive data on the regulation of GLUT4 activity by 3-O-methyl-D-glucose.
Shamni, Ofer; Cohen, Guy; Gruzman, Arie; Zaid, Hilal; Klip, Amira; Cerasi, Erol; Sasson, Shlomo.
Afiliação
  • Shamni O; The Institute for Drug Research, Section of Pharmacology, Diabetes Research Unit, Faculty of Medicine, The Hebrew University, Jerusalem 9112102, Israel.
  • Cohen G; The Institute for Drug Research, Section of Pharmacology, Diabetes Research Unit, Faculty of Medicine, The Hebrew University, Jerusalem 9112102, Israel.
  • Gruzman A; The Institute for Drug Research, Section of Pharmacology, Diabetes Research Unit, Faculty of Medicine, The Hebrew University, Jerusalem 9112102, Israel.
  • Zaid H; Program in Cell Biology, Hospital for Sick Children, Toronto, OT, Canada M5G 1XB.
  • Klip A; Program in Cell Biology, Hospital for Sick Children, Toronto, OT, Canada M5G 1XB.
  • Cerasi E; Endocrinology and Metabolism Service, Department of Internal Medicine, The Hebrew University-Hadassah Medical Center, Jerusalem 9112001, Israel.
  • Sasson S; The Institute for Drug Research, Section of Pharmacology, Diabetes Research Unit, Faculty of Medicine, The Hebrew University, Jerusalem 9112102, Israel.
Data Brief ; 14: 329-336, 2017 Oct.
Article em En | MEDLINE | ID: mdl-28795110
ABSTRACT
The data presented in this article are related to the research article entitled "Regulation of GLUT4 activity in myotubes by 3-O-methyl-D-glucose" (Shamni et al., 2017) [1]. These data show that the experimental procedures used to analyze the effects of 3-O-methyl-D-glucose (MeGlc) on the rate of hexose transport into myotubes were valid and controlled. The stimulatory effect of MeGlc was limited to glucose transporter 4 (GLUT4) and was independent of ambient glucose and protein synthesis. Cornish-Bowden kinetic analysis of uptake data revealed that MeGlc attenuated indinavir-induced inhibition of hexose transport in a competitive manner.
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Texto completo: 1 Coleções: 01-internacional Base de dados: MEDLINE Idioma: En Revista: Data Brief Ano de publicação: 2017 Tipo de documento: Article

Texto completo: 1 Coleções: 01-internacional Base de dados: MEDLINE Idioma: En Revista: Data Brief Ano de publicação: 2017 Tipo de documento: Article