Wanlaya UthaisangLeta K. NuttSten OrreniusBengt FadeelKarolinska InstitutetMahidol University2018-07-242018-07-242003-06-19FEBS Letters. Vol.545, No.2-3 (2003), 110-114001457932-s2.0-0038202902https://repository.li.mahidol.ac.th/handle/123456789/20718Previous studies have demonstrated that Fas-triggered activation of effector caspases and subsequent nuclear apoptosis either is mitochondria-independent (type I cells) or relies on mitochondrial amplification of the initial stimulus (type II cells). We show herein that Bcl-2 overexpression in a prototypic type I cell line (SKW6.4) promotes mitochondrial generation of ATP and blocks Fas-triggered plasma membrane externalization of phosphatidylserine (PS). Moreover, overexpression of Bcl-2 attenuates macrophage engulfment of Fas-triggered cells. Fas-mediated DNA fragmentation, on the other hand, remains unaffected in SKW6.4-bcl-2 cells. These studies thus demonstrate that PS externalization and clearance of cell corpses are mitochondria-dependent events, and show that these events can be dissociated from other features of the apoptotic program, in Fas type I cells. © 2003 Federation of European Biochemical Societies. Published by Elsevier Science B.V. All rights reserved.Mahidol UniversityBiochemistry, Genetics and Molecular BiologyPhosphatidylserine exposure in Fas type I cells is mitochondria-dependentArticleSCOPUS10.1016/S0014-5793(03)00508-8