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http://purl.uniprot.org/citations/27838822http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/27838822http://www.w3.org/2000/01/rdf-schema#comment"The c-Jun N-terminal kinase-mitogen-activated protein kinase (JNK-MAPK) pathway assists in modulating signals for growth, survival, and metabolism, thereby coordinating many cellular events during normal and stress conditions. To understand the role of the JNK-MAPK pathway during bacterial infection, an in vivo model organism Caenorhabditis elegans was used. In order to check the involvement of the JNK-MAPK pathway, the survival rate of C. elegans wild type (WT), and JNK-MAPK pathway mutant worms' upon exposure to selective Gram-positive and Gram-negative pathogenic bacteria, was studied. Among the pathogens, Shigella flexneri M9OT was found to efficiently colonize inside the WT and JNK-MAPK pathway mutant worms. qPCR studies had suggested that the above pathway-specific genes kgb-2 and jnk-1 were prominently responsible for the immune response elicited by the host during the M9OT infection. In addition, daf-16, which is a major transcription factor of the insulin/insulin growth factor-1 signaling (IIS) pathway, was also found to be involved during the host response. Crosstalk between IIS and JNK-MAPK pathways has probably been involved in the activation of the host immune system, which consequently leads to lifespan extension. Furthermore, it is also observed that daf-16 activation by JNK-MAPK pathway leads to antimicrobial response, by activating lys-7 expression. These findings suggest that JNK-MAPK is not the sole pathway that enhances the immunity of the host. Nonetheless, the IIS pathway bridges the JNK-MAPK pathway that influences in protecting the host in counter to the M9OT infection."xsd:string
http://purl.uniprot.org/citations/27838822http://purl.org/dc/terms/identifier"doi:10.1007/s12026-016-8879-6"xsd:string
http://purl.uniprot.org/citations/27838822http://purl.uniprot.org/core/author"Balamurugan K."xsd:string
http://purl.uniprot.org/citations/27838822http://purl.uniprot.org/core/author"Marudhupandiyan S."xsd:string
http://purl.uniprot.org/citations/27838822http://purl.uniprot.org/core/date"2017"xsd:gYear
http://purl.uniprot.org/citations/27838822http://purl.uniprot.org/core/name"Immunol Res"xsd:string
http://purl.uniprot.org/citations/27838822http://purl.uniprot.org/core/pages"609-621"xsd:string
http://purl.uniprot.org/citations/27838822http://purl.uniprot.org/core/title"Intrinsic JNK-MAPK pathway involvement requires daf-16-mediated immune response during Shigella flexneri infection in C. elegans."xsd:string
http://purl.uniprot.org/citations/27838822http://purl.uniprot.org/core/volume"65"xsd:string
http://purl.uniprot.org/citations/27838822http://www.w3.org/2004/02/skos/core#exactMatchhttp://purl.uniprot.org/pubmed/27838822
http://purl.uniprot.org/citations/27838822http://xmlns.com/foaf/0.1/primaryTopicOfhttps://pubmed.ncbi.nlm.nih.gov/27838822
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http://purl.uniprot.org/uniprot/#_O16850-mappedCitation-27838822http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/27838822
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http://purl.uniprot.org/uniprot/O16850http://purl.uniprot.org/core/mappedCitationhttp://purl.uniprot.org/citations/27838822
http://purl.uniprot.org/uniprot/A0A0K3AR63http://purl.uniprot.org/core/mappedCitationhttp://purl.uniprot.org/citations/27838822
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