This Article Full Text Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Reprints and Permissions Copyright Information Books from ASM Press MicrobeWorld Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Liu, H. Articles by Yang-Yen, H.-F. Search for Related Content PubMed PubMed Citation Articles by Liu, H. Articles by Yang-Yen, H.-F.

Stabilization and Enhancement of the Antiapoptotic Activity of Mcl-1 by TCTP

Institute of Molecular Medicine, National Taiwan University Medical School,¹ Institute of Molecular Biology, Academia Sinica, Taipei, Taiwan²

Received 9 September 2004/ Returned for modification 25 October 2004/ Accepted 12 January 2005

Mcl-1 is one Bcl-2 family member that plays a pivotal role in animal development. The extremely labile nature of the Mcl-1 protein itself and the fact that the Mcl-1 level is a critical determinant in various cell survival pathways suggest that cellular processes that regulate Mcl-1 stability are as important as those that regulate Mcl-1 synthesis. Although transcriptional stimulation of Mcl-1 synthesis in response to various stimuli has been well documented, regulation of Mcl-1 stability has been hardly explored. In this study, we identified that the translationally controlled tumor protein (TCTP) was one cellular factor that interacted with Mcl-1 and modulated Mcl-1 stability. While overexpression of TCTP augmented the protein stability of Mcl-1, knockdown expression of TCTP by RNA interference destabilized Mcl-1. Furthermore, TCTP stabilized Mcl-1 through interfering with Mcl-1's degradation by the ubiquitin-dependent proteasome degradation pathway, and the TCTP binding-defective mutant of Mcl-1 (K257V) was much more susceptible to degradation and manifested a compromised antiapoptotic activity. Taken together, these results suggest that TCTP modulates Mcl-1's antiapoptotic activity by modulating its protein stability. The possible mechanism(s) involved in TCTP's modulation process is discussed.

This article has been cited by other articles:

• Tait, S. W.G., de Vries, E., Maas, C., Keller, A. M., D'Santos, C. S., Borst, J. (2007). Apoptosis induction by Bid requires unconventional ubiquitination and degradation of its N-terminal fragment. J. Cell Biol. 179: 1453-1466 [Abstract] [Full Text]  
• De Biasio, A., Vrana, J. A., Zhou, P., Qian, L., Bieszczad, C. K., Braley, K. E., Domina, A. M., Weintraub, S. J., Neveu, J. M., Lane, W. S., Craig, R. W. (2007). N-terminal Truncation of Antiapoptotic MCL1, but Not G2/M-induced Phosphorylation, Is Associated with Stabilization and Abundant Expression in Tumor Cells. J. Biol. Chem. 282: 23919-23936 [Abstract] [Full Text]  
• Lin, K.-R., Lee, S.-F., Hung, C.-M., Li, C.-L., Yang-Yen, H.-F., Yen, J. J. Y. (2007). Survival Factor Withdrawal-induced Apoptosis of TF-1 Cells Involves a TRB2-Mcl-1 Axis-dependent Pathway. J. Biol. Chem. 282: 21962-21972 [Abstract] [Full Text]  
• Chen, S. H., Wu, P.-S., Chou, C.-H., Yan, Y.-T., Liu, H., Weng, S.-Y., Yang-Yen, H.-F. (2007). A Knockout Mouse Approach Reveals that TCTP Functions as an Essential Factor for Cell Proliferation and Survival in a Tissue- or Cell Type-specific Manner. Mol. Biol. Cell 18: 2525-2532 [Abstract] [Full Text]  
• Chou, C.-H., Lee, R.-S., Yang-Yen, H.-F. (2006). An Internal EELD Domain Facilitates Mitochondrial Targeting of Mcl-1 via a Tom70-dependent Pathway. Mol. Biol. Cell 17: 3952-3963 [Abstract] [Full Text]