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Microglial-specific depletion of TAK1 is neuroprotective in the acute phase after ischemic stroke
AbstractTransforming growth factor- β-activated kinase 1 (TAK1) is upregulated after cerebral ischemia and contributes to an aggravation of brain injury. TAK1 acts as a key regulator of NF-ΚB and the MAP kinases JNK and p38 and modulates post-ischemic neuroinflammation and apoptosis. Microglia are the main TAK1-expressing immunocomp etent cells of the brain. However, little is known about the function and regulation of microglial TAK1 after cerebral ischemia. Tamoxifen-dependent conditional depletion of TAK1 in microglial cells was induced inCx3cr1creER-Tak1fl/fl mice. ThecreER-negativeTak1fl/fl mice and vehicle-treated ...
Source: Journal of Molecular Medicine - May 6, 2020 Category: Molecular Biology Source Type: research