Interaction between fortilin and transforming growth factor-beta stimulated clone-22 (TSC-22) prevents apoptosis via the destabilization of TSC-22
Abstract
Yeast two-hybrid screening was conducted using a human ovary cDNA library to search for a novel binding protein using transforming growth factor-beta stimulated clone-22 (TSC-22). The selected protein was fortilin, which has been characterized as a nuclear anti-apoptotic protein. Overexpression of fortilin in ovarian carcinoma cells reversed TSC-22-mediated apoptosis, and the inhibition of fortilin expression via small interfering RNA (siRNA) resulted in an increase in the apoptosis of ovarian carcinoma cells. Moreover, fortilin overexpression promoted the degradation of TSC-22. Thus, an interaction between fortilin and TSC-22 prevents apoptosis via the destabilization of TSC-22 in ovarian carcinoma cells.
Structured summary
Abbreviations: DAPI, 4,6′-diamidino-2-phenylindole, GST, glutathione S-transferase, ONPG, o-nitrophenyl β-d-galactopyranoside, sifortilin, siRNA, small interfering RNA, THG-1, TSC-22 homologous gene-1, TSC-22, transforming growth factor-beta stimulated clone-22
Keywords: Apoptosis, Fortilin, Ovarian carcinoma cell, TSC-22, Yeast two hybrid
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PII: S0014-5793(08)00171-3
doi:10.1016/j.febslet.2008.01.066
© 2008 Federation of European Biochemical Societies
Refers to corrigendum:
- Corrigendum to “Interaction between fortilin and transforming growth factor-beta stimulated clone-22 (TSC-22) prevents apoptosis via the destabilization of TSC-22” [FEBS Lett. 582 (2008) 1210–1218] , 11 February 2009
