期刊
MEDICINAL RESEARCH REVIEWS
卷 36, 期 2, 页码 313-341出版社
WILEY-BLACKWELL
DOI: 10.1002/med.21379
关键词
Bcl-2 family proteins; apoptosis; Bax activators; drug discovery; cancer therapy
资金
- National Institutes of Health [P30 DA028821, R01 DA038446]
- Gulf Coast Consortia (GCC) [T32 GM089657]
- John Sealy Memorial Endowment Fund
- Institute for Translational Sciences (ITS)
- Sealy Center for Molecular Medicine
- Center for Addiction Research (CAR)
Bax, a central cell death regulator, is an indispensable gateway to mitochondrial dysfunction and a major proapoptotic member of the B-cell lymphoma 2 (Bcl-2) family proteins that control apoptosis in normal and cancer cells. Dysfunction of apoptosis renders the cancer cell resistant to treatment as well as promotes tumorigenesis. Bax activation induces mitochondrial membrane permeabilization, thereby leading to the release of apoptotic factor cytochrome c and consequently cancer cell death. A number of drugs in clinical use are known to indirectly activate Bax. Intriguingly, recent efforts demonstrate that Bax can serve as a promising direct target for small-molecule drug discovery. Several direct Bax activators have been identified to hold promise for cancer therapy with the advantages of specificity and the potential of overcoming chemo- and radioresistance. Further investigation of this new class of drug candidates will be needed to advance them into the clinic as a novel means to treat cancer.
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