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dc.contributor.authorSluss, Hayla Karen
dc.contributor.authorHan, Zhiqiang
dc.contributor.authorBarrett, Tamera
dc.contributor.authorGoberdhan, Deborah C. I.
dc.contributor.authorWilson, Clive
dc.contributor.authorDavis, Roger J.
dc.contributor.authorIp, Y. Tony
dc.date2022-08-11T08:08:48.000
dc.date.accessioned2022-08-23T16:08:54Z
dc.date.available2022-08-23T16:08:54Z
dc.date.issued1996-11-01
dc.date.submitted2009-01-12
dc.identifier.citation<p>Genes Dev. 1996 Nov 1;10(21):2745-58.</p>
dc.identifier.issn0890-9369 (Print)
dc.identifier.doi10.1101/gad.10.21.2745
dc.identifier.pmid8946915
dc.identifier.urihttp://hdl.handle.net/20.500.14038/32563
dc.description.abstractThe Drosophila MAP kinase DJNK is a homolog of the mammalian c-Jun amino-terminal kinase (JNK). Mutations in the DJNK gene correspond to the complementation group basket. DJNK is phosphorylated and activated by the Drosophila MAP kinase kinase HEP. Substrates of DJNK include the transcription factor DJun. DJNK participates in multiple physiological processes. Exposure to endotoxic lipopolysaccharide initiates an insect immune response and leads to DJNK activation. In addition, embryos lacking DJNK are defective in dorsal closure, a process in which the lateral epithelial cells migrate over the embryo and join at the dorsal midline. These data demonstrate that the DJNK signal transduction pathway mediates an immune response and morphogenesis in vivo.
dc.language.isoen_US
dc.relation<p><a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&list_uids=8946915&dopt=Abstract">Link to Article in PubMed</a></p>
dc.relation.urlhttps://doi.org/10.1101/gad.10.21.2745
dc.subjectAlleles; Amino Acid Sequence; Animals; Base Sequence; DNA, Complementary; Drosophila; *Drosophila Proteins; Gene Expression Regulation, Developmental; Gene Expression Regulation, Enzymologic; Mitogen-Activated Protein Kinase Kinases; Molecular Sequence Data; Morphogenesis; Phenotype; Phosphorylation; Protein Kinases; Sequence Homology, Amino Acid; *Signal Transduction; Substrate Specificity
dc.subjectLife Sciences
dc.subjectMedicine and Health Sciences
dc.titleA JNK signal transduction pathway that mediates morphogenesis and an immune response in Drosophila
dc.typeJournal Article
dc.source.journaltitleGenes and development [added]
dc.source.volume10
dc.source.issue21
dc.identifier.legacycoverpagehttps://escholarship.umassmed.edu/gsbs_sp/1127
dc.identifier.contextkey692118
html.description.abstract<p>The Drosophila MAP kinase DJNK is a homolog of the mammalian c-Jun amino-terminal kinase (JNK). Mutations in the DJNK gene correspond to the complementation group basket. DJNK is phosphorylated and activated by the Drosophila MAP kinase kinase HEP. Substrates of DJNK include the transcription factor DJun. DJNK participates in multiple physiological processes. Exposure to endotoxic lipopolysaccharide initiates an insect immune response and leads to DJNK activation. In addition, embryos lacking DJNK are defective in dorsal closure, a process in which the lateral epithelial cells migrate over the embryo and join at the dorsal midline. These data demonstrate that the DJNK signal transduction pathway mediates an immune response and morphogenesis in vivo.</p>
dc.identifier.submissionpathgsbs_sp/1127
dc.contributor.departmentProgram in Molecular Medicine
dc.contributor.departmentDepartment of Biochemistry and Molecular Biology
dc.contributor.departmentGraduate School of Biomedical Sciences
dc.source.pages2745-58


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