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Cell death regulation by B-cell lymphoma protein.
Verma, Y K; Gangenahalli, G U; Singh, V K; Gupta, P; Chandra, R; Sharma, R K; Raj, H G.
Affiliation
  • Verma YK; Stem Cell Gene Therapy Research Group, Lucknow Road, Timar Pur, Delhi, 110054, India.
Apoptosis ; 11(4): 459-71, 2006 Apr.
Article in En | MEDLINE | ID: mdl-16547596
Bcl-2 (B Cell Lymphoma) protein is an anti-apoptotic member of Bcl-2 family, which is comprised of pro- and anti-apoptotic members. It regulates cellular proliferation and death by inter- and intra-family interactions. It has a potential to suppress apoptotic cell death under variety of stress conditions by modulating mitochondrial transmembrane potential. However, prevalence of constitutively activated Bcl-2 cellular activity is not always required in cells; a mechanism likely exists in cells, which controls its activity. When expression of Bcl-2 is unregulated, it generates lymphoma like, follicular B-cell lymphoma. This article reviews the structural and functional regulation of Bcl-2 activity at transcriptional, translational, domain, structural and post-translational level, which also accounts for the effects of its deletion and site-directed mutants in the regulation of cellular proliferation and differentiation in vitro and in vivo. This concisely reviewed information on Bcl-2 helps us to update our understanding of cell death and its modulation by Bcl-2 and its mutant's interaction, which has gained therapeutic benefits in cell growth and proliferation, particularly for sensitive human hematopoietic stem cells.
Subject(s)
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Collection: 01-internacional Database: MEDLINE Main subject: Apoptosis / Proto-Oncogene Proteins c-bcl-2 Type of study: Risk_factors_studies Limits: Animals Language: En Journal: Apoptosis Year: 2006 Document type: Article Affiliation country: Country of publication:
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Collection: 01-internacional Database: MEDLINE Main subject: Apoptosis / Proto-Oncogene Proteins c-bcl-2 Type of study: Risk_factors_studies Limits: Animals Language: En Journal: Apoptosis Year: 2006 Document type: Article Affiliation country: Country of publication: