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SWI/SNF chromatin remodelling complex and retroviral gene silencing.
Iba, Hideo; Mizutani, Taketoshi; Ito, Taiji.
Afiliação
  • Iba H; Division of Host-Parasite Interaction, Department of Microbiology and Immunology, Institute of Medical Science, University of Tokyo, 4-6-1 Shirokanedai, Minato-ku, Tokyo 108-8639, Japan. iba@ims.u-tokyo.ac.jp
Rev Med Virol ; 13(2): 99-110, 2003.
Article em En | MEDLINE | ID: mdl-12627393
ABSTRACT
Because of the unique infectious cycle of retroviruses which involves the integration of the retroviral genome into the host chromosome, many cellular chromosomal proteins are used by the virus to maintain its gene expression. At the same time, cellular mechanisms for the surveillance and exclusion of non-self expression by such intragenomic parasites operate as an important host defence system in the cellular nuclei. Retroviruses have strategies for escaping from host defence systems, such as by maintaining or reactivating viral expression in specific host cell types. Understanding such epigenetical regulation would be essential for progress in retroviral virology. In this review, we emphasise the importance of the chromatin remodelling factor SWI/SNF complex as one of the key players in epigenetic regulation of host and viral gene expression. An understanding of these mechanisms will surely lead to new ideas on the pathogenicity of this virus, on the latent infection observed in many other viruses, and further forward the design of unique retroviral vectors for long-term transgene expression, providing strong tools for human gene therapy and regenerative medicine.
Assuntos
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Coleções: 01-internacional Base de dados: MEDLINE Assunto principal: Retroviridae / Fatores de Transcrição / Cromatina / Proteínas Cromossômicas não Histona / Inativação Gênica Limite: Humans Idioma: En Ano de publicação: 2003 Tipo de documento: Article
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Coleções: 01-internacional Base de dados: MEDLINE Assunto principal: Retroviridae / Fatores de Transcrição / Cromatina / Proteínas Cromossômicas não Histona / Inativação Gênica Limite: Humans Idioma: En Ano de publicação: 2003 Tipo de documento: Article