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MAP kinase activation

Transduction mechanism Inhibition of adenylyl cyclase stimulation of tyrosine phosphatase activity stimulation of MAP kinase activity activation of ERK inhibition of Ca2+ channel activation stimulation of Na+/H+ exchanger stimulation of AM PA/kainate glutamate channels Inhibition of forskol in-stimulated adenylyl cyclase activation of phos-phoinositide metabolism stimulation of tyrosine phosphatase activity inhibition of Ca2+ channel activation activation of K+ channel inhibition of AM PA/ kainate glutamate channels inhibition of MAP kinase activity inhibition of ERK stimulation of SHP-1 and SHP-2 Inhibition of adenylyl cyclase stimulation of phosphoinositide metabolism stimulation of tyrosine phosphatase activation of K+ channel inhibi-tion/stimulation of MAP kinase activity induction of p53 and Bax Inhibition of adenylyl cyclase stimulation of MAP kinase stimulation of p38 activation of tyrosine phosphatase stimulation of K+ channels and phospholipase A2 Inhibition of adenylyl cyclase activation/ inhibition of phosphoinositide metabolism inhibition of Ca2+ influx activation of K+ channels inhibition of MAP kinase stimulation of tyrosine phosphatase... [Pg.1150]

Kosako, H Gotoh, Y Matsuda, S Ishikawa, M and Nishida, E. (1992). Xenopus MAP kinase activator is a serine/threonine/tyrosine kinase activated by threonine phosphorylation. EMBO J. 11 2903-2908. [Pg.43]

Nakielny, S., Cohen, P., Wu, J., and Sturgill, T. (1992a). MAP kinase activator from insulin-stimulated skeletal muscle is a protein serine/threonine kinase. EMBO S. 11 2123-2129. [Pg.47]

The relationship between MAP kinase activity and/or its direct substrates (e.g. p90rsk) and CSF inactivation is unclear. Abrieu and colleagues (1996) found that in cell-free Xenopus eggs extracts MAP kinase remains active when MPF is inactivated. Thus, despite the fact that MAP kinase remains continuously active and phosphorylated, the CSF activity seems to be inactivated. A similar pattern... [Pg.82]

Verlhac MH, de Pennart H, Maro B, Cobb MH, Clarke HJ 1993 MAP kinase becomes stably activated at metaphase and is associated with microtubule-organizing centers during meiotic maturation of mouse oocytes. Dev Biol 158 330-340 Verlhac MH, Kubiak JZ, Clarke HJ, Maro B 1994 Microtubule and chromatin behavior follow MAP kinase activity but not MPF activity during meiosis in mouse oocytes. Development 120 1017-1025... [Pg.89]

MAP kinase-activated protein kinases (e,g., Mnkl, p90RSKs)... [Pg.154]

MK2 (also termed MAP kinase-activated protein kinase 2, MAPKAP-K2) is activated by p38 MAP kinase a// (Kotlyarov et al, 2002 Roux and Blenis, 2004). MK2 plays a key role in the control of the production of certain cytokines, for example, tumor necrosis factor a. MK2 does so by phosphorylating proteins that bind specifically to the regulatory regions in the S untranslated regions (UTRs) of such mRNAs (Hitti et al, 2006). These regions contain AU-rich elements (AREs) to which proteins such as HnRNP A1 also bind. [Pg.155]

Sutherland, C., Alterio, J., Campbell, D. G., Le Bourdelles, B., Mallet, J., Haavik, J., and Cohen, P. (1993). Phosphorylation and activation of human tyrosine hydroxylase in vitro by mitogen-activated protein (MAP) kinase and MAP-kinase-activated kinases 1 and 2. Em.J. Biodiem. 217, 715-722. [Pg.175]

Sutherland, C., and Cohen, P. (1994). The alpha-isoform of glycogen synthase kinase-3 from rabbit skeletal muscle is inactivated by p70 S6 kinase or MAP kinase-activated protein kinase-1 in vitro. FEBS Lett. 338, 37—42. [Pg.175]

Knowles, R. B., Chin, J., Ruff, C. T. and Hyman, B. T. (1999). Demonstration by fluorescence resonance energy transfer of a close association between activated MAP kinase and neurofibrillary tangles Implications for MAP kinase activation in Alzheimer disease. J. Neuropathol. Exp. Neurol. 58, 1090-8. [Pg.66]

MAPKAP MAP-kinase-activated protein kinase NHE Na+/H+ antiporter... [Pg.965]

Gupta, A., Rosenberger, S. F., and Bowden, G. T., Increased ROS levels contribute to elevated transcription factor and MAP kinase activities in malignantly progressed mouse keratinocyte cell lines, Carcinogenesis, 20, 2063, 1999. [Pg.289]

Laskin, J. D., Heck D.E., and Laskin D.L. The ribotoxic stress response as a potential mechanism for MAP kinase activation in xenobiotic toxicity. Toxicol. Sci. 69, 289, 2002. [Pg.303]

Dubey RK, Gillespie DG, Imthurn B et al. Phytoestrogens inhibit growth and MAP kinase activity in human aortic smooth muscle cells. Hypertension 33, 177-182, 1999. [Pg.395]

Van Biesen, T., Hawes, B.E., LuttreU, D.K., Krueger, K.M., Touhara, K., Porfiri, E., Sakaue, M., Luttrell, L.M. and Lefkowitz, R.L. Receptor-tyrosine-kinase- and GBy-mediated MAP kinase activation by a common signalling pathway (1995) Nature 376, 781-784... [Pg.349]

A MAP kinase module is composed of three kinases where MAP kinase kinase kinase (MAPKKK) will phosphorylate and induce a MAP kinase kinase (MAPKK), which will then phosphorylate and activate a MAP kinase. MAP kinase phosphory-lates either transcription factors that are nonkinase proteins or other kinases that are called MAP kinase-activating protein kinases (MK). There are four distinct classes of MAP kinases, which include ERKs, C-Jun-N-terminal kinases, p38 isoforms and ERK5. [Pg.75]

Ji, R. R., Befort, K., Brenner, G.J., and Woolf, C.J. (2002). ERK MAP kinase activation in superficial spinal cord neurons induced prodynorphine and NK-1 upregulation and contributes to persistent inflammatory pain hypersensitivity. J. Neurosci. 22, 478—485. [Pg.215]

Fig. 1.7 Possible mechanisms involving angiotensin II, oxidative stress and nitric oxide in enhanced Gi oc protein expression in hypertension. Gi protein expression is enhanced in genetic (SHR) and experimental hypertension including 1 kidney 1 clip (1K1C) and L-NAME-induced hypertension. Inhibition of nitric oxide synthase (NOS) by L-NAME activates renin angiotensin system, and also decreases the level of NO. 1K1C hypertensive rats also exhibit enhanced levels of Ang II. Ang II increases oxidative stress that through increased MAP kinase activity results in enhanced expression of Gi oc proteins and thereby hypertension. On the other hand, increased levels of NO and cGMP decrease the expression of Gia proteins in VSMC which may be an additional mechanism through which NO decreases blood pressure in L-NAME-induced hypertensive rats. Fig. 1.7 Possible mechanisms involving angiotensin II, oxidative stress and nitric oxide in enhanced Gi oc protein expression in hypertension. Gi protein expression is enhanced in genetic (SHR) and experimental hypertension including 1 kidney 1 clip (1K1C) and L-NAME-induced hypertension. Inhibition of nitric oxide synthase (NOS) by L-NAME activates renin angiotensin system, and also decreases the level of NO. 1K1C hypertensive rats also exhibit enhanced levels of Ang II. Ang II increases oxidative stress that through increased MAP kinase activity results in enhanced expression of Gi oc proteins and thereby hypertension. On the other hand, increased levels of NO and cGMP decrease the expression of Gia proteins in VSMC which may be an additional mechanism through which NO decreases blood pressure in L-NAME-induced hypertensive rats.
Rousseau S, Houle F, Landry J, Huot J. p38 MAP kinase activation by vascular endothelial growth factor mediates actin reorganization and cell migration in human endothelial cells. Oncogene 1997 15 2169-2177. [Pg.213]

Alemany, R., Sichelschmidt, B., Meyer zu Heringdorf, D.M., Lass, H., Van Koppen, CJ. and Jakobs, K.H., 2000, Stimulation of sphingosine 1-phosphate formation by theP2Y2 receptor in HL-60 cells Ca2+ requirement and implication in receptor-mediated Ca2+ mobilization, but not MAP kinase activation, Mol. Pharmacol. 58 491-497. [Pg.260]


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See also in sourсe #XX -- [ Pg.393 ]




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