Differential inhibitory effects of CrmA, P35, IAP and three mammalian IAP homologues on apoptosis in NIH3T3 cells following various death stimuli (original) (raw)
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- Published: 01 October 1997
Cell Death & Differentiation volume 4, pages 570–579 (1997)Cite this article
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Abstract
We have investigated the effects of expression of the viral proteins CrmA, P35 and IAP, and the three mammalian IAP homologues (MIHA, MIHB and MIHC), on the regulation of apoptosis induced by either the overexpression of caspases (ICE, CPP32 and Nedd2), by serum-deprivation, or by γ-irradiation in NIH3T3 fibroblasts. As previously shown, CrmA strongly inhibited ICE-induced apoptosis but was ineffective against Nedd2- or CPP32-mediated apoptosis. P35, IAP and MIHA protected cells from apoptosis induced by the three caspases to varying extents but MIHB and MIHC were largely ineffective. NIH3T3 cells expressing P35 and MIHA, but not IAP, CrmA, MIHB and MIHC, showed enhanced cell survival under serum-deprived conditions. In addition, P35, CrmA and MIHA could provide substantial protection against death induced by γ-irradiation. These results suggest the presence of multiple apoptotic pathways with differential sensitivity to various naturally occurring apoptosis inhibitors.
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- Hanson Centre for Cancer Research, Institute of Medical and Veterinary Science, PO Box 14, Rundle Mall, SA 5000, Adelaide, Australia
Loretta Dorstyn & Sharad Kumar
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- Loretta Dorstyn
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Correspondence toSharad Kumar.
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Dorstyn, L., Kumar, S. Differential inhibitory effects of CrmA, P35, IAP and three mammalian IAP homologues on apoptosis in NIH3T3 cells following various death stimuli.Cell Death Differ 4, 570–579 (1997). https://doi.org/10.1038/sj.cdd.4400281
- Received: 18 December 1997
- Revised: 18 March 1999
- Accepted: 19 May 1999
- Issue Date: 01 October 1997
- DOI: https://doi.org/10.1038/sj.cdd.4400281