The BH3 alpha-helical mimic BH3-M6 disrupts Bcl-X(L), Bcl-2, and MCL-1 protein-protein interactions with Bax, Bak, Bad, or Bim and induces apoptosis in a Bax- and Bim-dependent manner.

A critical hallmark of cancer cell survival is evasion of apoptosis. This is commonly due to overexpression of anti-apoptotic proteins such as Bcl-2, Bcl-X(L), and Mcl-1, which bind to the BH3 α-helical domain of pro-apoptotic proteins such as Bax, Bak, Bad, and Bim, and inhibit their function. We d...

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Bibliographic Details
Main Authors: Kazi, A, Sun, J, Doi, K, Sung, S, Takahashi, Y, Yin, H, Rodriguez, J, Becerril, J, Berndt, N, Hamilton, A, Wang, H, Sebti, S
Format: Journal article
Language:English
Published: 2011