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The role of human endogenous retroviruses in brain development and function.
Mortelmans, Kristien; Wang-Johanning, Feng; Johanning, Gary L.
  • Mortelmans K; Discovery Biology Section, Biosciences Division, SRI International, Menlo Park, CA, USA.
  • Wang-Johanning F; Discovery Biology Section, Biosciences Division, SRI International, Menlo Park, CA, USA.
  • Johanning GL; Discovery Biology Section, Biosciences Division, SRI International, Menlo Park, CA, USA.
APMIS ; 124(1-2): 105-15, 2016.
Article en En | MEDLINE | ID: mdl-26818265
ABSTRACT
Endogenous retroviral sequences are spread throughout the genome of all humans, and make up about 8% of the genome. Despite their prevalence, the function of human endogenous retroviruses (HERVs) in humans is largely unknown. In this review we focus on the brain, and evaluate studies in animal models that address mechanisms of endogenous retrovirus activation in the brain and central nervous system (CNS). One such study in mice found that TRIM28, a protein critical for mouse early development, regulates transcription and silencing of endogenous retroviruses in neural progenitor cells. Another intriguing finding in human brain cells and mouse models was that endogenous retrovirus HERV-K appears to be protective against neurotoxins. We also report on studies that associate HERVs with human diseases of the brain and CNS. There is little doubt of an association between HERVs and a number of CNS diseases. However, a cause and effect relationship between HERVs and these diseases has not yet been established.
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Texto completo: 1 Banco de datos: MEDLINE Asunto principal: Encéfalo / Encefalopatías / Retrovirus Endógenos Tipo de estudio: Etiology_studies / Prognostic_studies / Risk_factors_studies Límite: Animals / Humans Idioma: En Año: 2016 Tipo del documento: Article

Texto completo: 1 Banco de datos: MEDLINE Asunto principal: Encéfalo / Encefalopatías / Retrovirus Endógenos Tipo de estudio: Etiology_studies / Prognostic_studies / Risk_factors_studies Límite: Animals / Humans Idioma: En Año: 2016 Tipo del documento: Article