FADD is essential for glucose uptake and survival of thymocytes

Biochem Biophys Res Commun. 2014 Aug 22;451(2):202-7. doi: 10.1016/j.bbrc.2014.07.092. Epub 2014 Jul 28.

Abstract

Fas-associated protein with death domain (FADD) has been implicated in T lymphocytes, but the nature of FADD-dependent mechanism in early T cell development has not been completely elucidated. In this study, using T-cell specific deletion mice, we observed that FADD deficiency in thymocytes led to increased apoptosis and reduced cell numbers, which may be attributed to the reduction of Glut1 expression and correspondingly decreased glucose uptake. Furthermore, an abnormal transduction of Akt signaling was discovered in FADD(-/-) thymocytes, which may be responsible for the declined Glut1 expression. Collectively, our results demonstrate the new function of FADD in glucose metabolism and survival of early T cells.

Keywords: Akt; FADD; Glucose uptake; Glut1; Thymocytes.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Apoptosis
  • Biological Transport, Active
  • Cell Differentiation
  • Cell Survival
  • Cells, Cultured
  • Fas-Associated Death Domain Protein / deficiency
  • Fas-Associated Death Domain Protein / genetics
  • Fas-Associated Death Domain Protein / metabolism*
  • Glucose / metabolism*
  • Glucose Transporter Type 1 / metabolism
  • Mice
  • Mice, Knockout
  • Models, Biological
  • Proto-Oncogene Proteins c-akt / metabolism
  • Signal Transduction
  • T-Lymphocytes / cytology*
  • T-Lymphocytes / metabolism*

Substances

  • Fadd protein, mouse
  • Fas-Associated Death Domain Protein
  • Glucose Transporter Type 1
  • Slc2a1 protein, mouse
  • Proto-Oncogene Proteins c-akt
  • Glucose