ITM2BS regulates apoptosis by inducing loss of mitochondrial membrane potential

Eur J Immunol. 2002 Dec;32(12):3498-505. doi: 10.1002/1521-4141(200212)32:12<3498::AID-IMMU3498>3.0.CO;2-C.

Abstract

Apoptosis is a conserved and essential feature of homeostasis. We have found that expression of the short form of integral membrane protein 2B (ITM2B(S)) in IL-2-stimulated T cells, as well as in COS-7 cells, induces apoptosis. Biochemical and confocal studies demonstrate that association of ITM2B(S) with mitochondria correlates with loss of mitochondrial membrane potential, release of cytochrome c to the cytosol and, as a final consequence, induction of apoptosis in IL-2-stimulated cells. Moreover, the apoptosis-inducing activity of ITM2B(S) correlates with caspase 9 and caspase 3 activation. Taken together, our results demonstrate that ITM2B(S) induces apoptosis via a caspase-dependent mitochondrial pathway.

MeSH terms

  • Adaptor Proteins, Signal Transducing
  • Animals
  • Apoptosis / physiology*
  • COS Cells
  • Caspase 3
  • Caspase 9
  • Caspases / metabolism
  • Cell Line
  • Cytochrome c Group / metabolism
  • Membrane Potentials
  • Membrane Proteins / genetics
  • Membrane Proteins / physiology*
  • Mice
  • Mitochondria / metabolism*
  • T-Lymphocytes / cytology
  • T-Lymphocytes / physiology
  • Transfection

Substances

  • Adaptor Proteins, Signal Transducing
  • Cytochrome c Group
  • Itm2b protein, mouse
  • Membrane Proteins
  • Casp3 protein, mouse
  • Casp9 protein, mouse
  • Caspase 3
  • Caspase 9
  • Caspases