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dc.contributor.authorSabio, Guadalupe
dc.contributor.authorDavis, Roger J.
dc.date2022-08-11T08:08:16.000
dc.date.accessioned2022-08-23T15:48:57Z
dc.date.available2022-08-23T15:48:57Z
dc.date.issued2014-06-01
dc.date.submitted2016-03-09
dc.identifier.citationSemin Immunol. 2014 Jun;26(3):237-45. doi: 10.1016/j.smim.2014.02.009. Epub 2014 Mar 16. <a href="http://dx.doi.org/10.1016/j.smim.2014.02.009">Link to article on publisher's site</a>
dc.identifier.issn1044-5323 (Linking)
dc.identifier.doi10.1016/j.smim.2014.02.009
dc.identifier.pmid24647229
dc.identifier.urihttp://hdl.handle.net/20.500.14038/28320
dc.description.abstractThe binding of tumour necrosis factor alpha (TNFalpha) to cell surface receptors engages multiple signal transduction pathways, including three groups of mitogen-activated protein (MAP) kinases: extracellular-signal-regulated kinases (ERKs); the cJun NH2-terminal kinases (JNKs); and the p38 MAP kinases. These MAP kinase signalling pathways induce a secondary response by increasing the expression of several inflammatory cytokines (including TNFalpha) that contribute to the biological activity of TNFalpha. MAP kinases therefore function both upstream and down-stream of signalling by TNFalpha receptors. Here we review mechanisms that mediate these actions of MAP kinases during the response to TNFalpha.
dc.language.isoen_US
dc.relation<a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&list_uids=24647229&dopt=Abstract">Link to Article in PubMed</a>
dc.relation.urlhttp://www.ncbi.nlm.nih.gov/pmc/articles/PMC4099309/
dc.subjectAnimals
dc.subjectHumans
dc.subject*MAP Kinase Signaling System
dc.subjectTumor Necrosis Factor-alpha
dc.subjectERK
dc.subjectJNK
dc.subjectMAP kinase
dc.subjectTNF
dc.subjectp38 MAP kinase
dc.subjectBiochemistry
dc.subjectCell Biology
dc.subjectCellular and Molecular Physiology
dc.subjectMolecular Biology
dc.titleTNF and MAP kinase signalling pathways
dc.typeJournal Article
dc.source.journaltitleSeminars in immunology
dc.source.volume26
dc.source.issue3
dc.identifier.legacycoverpagehttps://escholarship.umassmed.edu/davis/48
dc.identifier.contextkey8293924
html.description.abstract<p>The binding of tumour necrosis factor alpha (TNFalpha) to cell surface receptors engages multiple signal transduction pathways, including three groups of mitogen-activated protein (MAP) kinases: extracellular-signal-regulated kinases (ERKs); the cJun NH2-terminal kinases (JNKs); and the p38 MAP kinases. These MAP kinase signalling pathways induce a secondary response by increasing the expression of several inflammatory cytokines (including TNFalpha) that contribute to the biological activity of TNFalpha. MAP kinases therefore function both upstream and down-stream of signalling by TNFalpha receptors. Here we review mechanisms that mediate these actions of MAP kinases during the response to TNFalpha.</p>
dc.identifier.submissionpathdavis/48
dc.contributor.departmentProgram in Molecular Medicine
dc.source.pages237-45


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