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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)

MEK1 protein kinase inhibition protects against damage resulting from focal cerebral ischemia.

The MEK1 (MAP kinase/ ERK kinase)/ERK (extracellular-signal-responsive kinase) pathway has been implicated in cell growth and differentiation [Seger, R. & Krebs, E. G. (1995) FASEB J. 9, 726-735]. Here we show that the MEK/ ERK pathway is activated during focal cerebral ischemia and may play a role in inducing damage. Treatment of mice 30 min before ischemia with the MEK1-specific inhibitor PD98059 [Alessi, D. R., Cuenda, A., Cohen, P. , Dudley, D. T. & Saltiel, A. R. (1995) J. Biol. Chem. 270, 27489-27494] reduces focal infarct volume at 22 hr after ischemia by 55% after transient occlusion of the middle cerebral artery. This is accompanied by a reduction in phospho-ERK1/2 immunohistochemical staining. MEK1 inhibition also results in reduced brain damage 72 hr after ischemia, with focal infarct volume reduced by 36%. This study indicates that the MEK1/ ERK pathway contributes to brain injury during focal cerebral ischemia and that PD98059, a MEK1-specific antagonist, is a potent neuroprotective agent.[1]


  1. MEK1 protein kinase inhibition protects against damage resulting from focal cerebral ischemia. Alessandrini, A., Namura, S., Moskowitz, M.A., Bonventre, J.V. Proc. Natl. Acad. Sci. U.S.A. (1999) [Pubmed]
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