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Journal article

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.

Abstract:

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 designed a BH3 α-helical mimetic BH3-M6 that binds to Bcl-X(L) and Mcl-1 and prevents their binding to fluorescently labeled Bak- or Bim-BH3 peptides in vitro. Using several approaches, we demonstra...

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Publication status:
Published

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Publisher copy:
10.1074/jbc.m110.203638

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Journal:
The Journal of biological chemistry
Volume:
286
Issue:
11
Pages:
9382-9392
Publication date:
2011-03-05
DOI:
EISSN:
1083-351X
ISSN:
0021-9258
URN:
uuid:a4bbeec4-39ed-4e4c-b795-8690bfae56a1
Source identifiers:
127287
Local pid:
pubs:127287

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