Sabio, GuadalupeDavis, Roger J.2022-08-232022-08-232014-06-012016-03-09Semin 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>1044-5323 (Linking)10.1016/j.smim.2014.02.00924647229https://hdl.handle.net/20.500.14038/28320The 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.en-USAnimalsHumans*MAP Kinase Signaling SystemTumor Necrosis Factor-alphaERKJNKMAP kinaseTNFp38 MAP kinaseBiochemistryCell BiologyCellular and Molecular PhysiologyMolecular BiologyJournal Articlehttps://escholarship.umassmed.edu/davis/488293924davis/48