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Gy 1999, 45:69-74.doi: 10.1186/1742-2094-7-36 Cite this article as: Talbot et al., Key role for spinal dorsal horn microglial kinin B1 receptor in early diabetic pain neuropathy Journal of Neuroinflammation 2010, 7:Wang et al. Journal of Neuroinflammation 2010, 7:84 http://www.jneuroinflammation.com/content/7/1/JOURNAL OF NEUROINFLAMMATIONRESEARCHOpen AccessCalmodulin kinase II-dependent tra
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Is. Moreover, matrix metalloproteinases (MMPs), MMP-9 especially, have been observed in patients with brain inflammatory diseases and may contribute to brain disease pathology. However, the molecular mechanisms underlying LTA-induced MMP-9 expression in brain astrocytes remain unclear. Objective: The goal of this study was to examine whether LTA-induced cell migration is mediated by calcium/ calmo
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Is. Moreover, matrix metalloproteinases (MMPs), MMP-9 especially, have been observed in patients with brain inflammatory diseases and may contribute to brain disease pathology. However, the molecular mechanisms underlying LTA-induced MMP-9 expression in brain astrocytes remain unclear. Objective: The goal of this study was to examine whether LTA-induced cell migration is mediated by calcium/ calmo
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Is. Moreover, matrix metalloproteinases (MMPs), MMP-9 especially, have been observed in patients with brain inflammatory diseases and may contribute to brain disease pathology. However, the molecular mechanisms underlying LTA-induced MMP-9 expression in brain astrocytes remain unclear. Objective: The goal of this study was to examine whether LTA-induced cell migration is mediated by calcium/ calmo
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Tion via a thiolester linkage to an internal cysteine in E1, which then transfers the ubiquitin to a cysteine residue of an E2 protein. The E2 interacts with an E3 to mediate covalent attachment of ubiquitin onto substrate proteins. Repeated rounds of E2/E3mediated ubiquitin transfer result in polyubiquitylation, allowing substrate proteins to be recognized and destroyed by the proteasome. Vertebr
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