Author: ["Oliver Herrmann","Bernd Baumann","Rossana de Lorenzi","Sajjad Muhammad","Wen Zhang","Jens Kleesiek","Max Malfertheiner","Martin Köhrmann","Ioana Potrovita","Ira Maegele","Cordian Beyer","James R Burke","Mazahir T Hasan","Hermann Bujard","Thomas Wirth","Manolis Pasparakis","Markus Schwaninger"]
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Abstract
The IκB kinase complex IKK is a central component of the signaling cascade that controls NF-κB–dependent gene transcription. So far, its function in the brain is largely unknown. Here, we show that IKK is activated in a mouse model of stroke. To investigate the function of IKK in brain ischemia we generated mice that contain a targeted deletion of Ikbkb (which encodes IKK2) in mouse neurons and mice that express a dominant inhibitor of IKK in neurons. In both lines, inhibition of IKK activity markedly reduced infarct size. In contrast, constitutive activation of IKK2 enlarged the infarct size. A selective small-molecule inhibitor of IKK mimicked the effect of genetic IKK inhibition in neurons, reducing the infarct volume and cell death in a therapeutic time window of 4.5 h. These data indicate a key function of IKK in ischemic brain damage and suggest a potential role for IKK inhibitors in stroke therapy.Cite this article
Herrmann, O., Baumann, B., de Lorenzi, R. et al. IKK mediates ischemia-induced neuronal death. Nat Med 11, 1322–1329 (2005). https://doi.org/10.1038/nm1323 