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A conserved PMK-1/p38 MAPK is required in caenorhabditis elegans tissue-specific immune response to Yersinia pestis infection.
Bolz, Devin D; Tenor, Jennifer L; Aballay, Alejandro.
Afiliação
  • Bolz DD; Department of Molecular Genetics and Microbiology, Duke University Medical Center, Durham, North Carolina 27710, USA.
J Biol Chem ; 285(14): 10832-40, 2010 Apr 02.
Article em En | MEDLINE | ID: mdl-20133945
Yersinia pestis has acquired a variety of complex strategies that enable the bacterium to overcome defenses in different hosts and ensure its survival and successful transmission. A full-genome microarray analysis on Caenorhabditis elegans infected with Y. pestis shows enrichment in genes that are markers of innate immune responses and regulated by a conserved PMK-1/p38 MAPK. Consistent with a role in regulating expression of immune effectors, inhibition of PMK-1/p38 by mutation or RNA interference enhances susceptibility to Y. pestis. Further studies of mosaic animals where PMK-1/p38 is exclusively inhibited or overexpressed in a tissue-specific manner indicate that PMK-1/p38 controls expression of a CUB-like family of immune genes at the cell-autonomous level. Given the conserved nature of PMK-1/p38 MAPK-mediated signaling and innate immune responses, PMK-1/p38 MAPK may play a role in the immune response against Y. pestis in natural hosts.
Assuntos

Texto completo: 1 Coleções: 01-internacional Base de dados: MEDLINE Assunto principal: Peste / Yersinia pestis / Caenorhabditis elegans / Proteínas Quinases Ativadas por Mitógeno / Proteínas de Caenorhabditis elegans / Proteínas Quinases p38 Ativadas por Mitógeno Limite: Animals Idioma: En Ano de publicação: 2010 Tipo de documento: Article

Texto completo: 1 Coleções: 01-internacional Base de dados: MEDLINE Assunto principal: Peste / Yersinia pestis / Caenorhabditis elegans / Proteínas Quinases Ativadas por Mitógeno / Proteínas de Caenorhabditis elegans / Proteínas Quinases p38 Ativadas por Mitógeno Limite: Animals Idioma: En Ano de publicação: 2010 Tipo de documento: Article