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Therapeutic Modulation of Apoptosis: Targeting the BCL-2 Family at the Interface of the Mitochondrial Membrane
Yonsei Medical Journal ; : 689-697, 2008.
Artículo en Inglés | WPRIM | ID: wpr-100116
ABSTRACT
A vast portion of human disease results when the process of apoptosis is defective. Disorders resulting from inappropriate cell death range from autoimmune and neurodegenerative conditions to heart disease. Conversely, prevention of apoptosis is the hallmark of cancer and confounds the efficacy of cancer therapeutics. In the search for optimal targets that would enable the control of apoptosis, members of the BCL-2 family of anti- and pro-apoptotic factors have figured prominently. Development of BCL-2 antisense approaches, small molecules, and BH3 peptidomimetics has met with both success and failure. Success-because BCL-2 proteins play essential roles in apoptosis. Failure-because single targets for drug development have limited scope. By examining the activity of the BCL-2 proteins in relation to the mitochondrial landscape and drawing attention to the significant mitochondrial membrane alterations that ensue during apoptosis, we demonstrate the need for a broader based multi-disciplinary approach for the design of novel apoptosis-modulating compounds in the treatment of human disease.
Asunto(s)

Texto completo: Disponible Índice: WPRIM (Pacífico Occidental) Asunto principal: Diseño de Fármacos / Transducción de Señal / Familia de Multigenes / Apoptosis / Proteínas Proto-Oncogénicas c-bcl-2 / Genes bcl-2 / Membranas Mitocondriales / Proteína Proapoptótica que Interacciona Mediante Dominios BH3 / Mitocondrias Límite: Humanos Idioma: Inglés Revista: Yonsei Medical Journal Año: 2008 Tipo del documento: Artículo

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Texto completo: Disponible Índice: WPRIM (Pacífico Occidental) Asunto principal: Diseño de Fármacos / Transducción de Señal / Familia de Multigenes / Apoptosis / Proteínas Proto-Oncogénicas c-bcl-2 / Genes bcl-2 / Membranas Mitocondriales / Proteína Proapoptótica que Interacciona Mediante Dominios BH3 / Mitocondrias Límite: Humanos Idioma: Inglés Revista: Yonsei Medical Journal Año: 2008 Tipo del documento: Artículo