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您的检索式：作者名="Christian Engelmann"
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| 1 | Role of nuclear factor kappa B in central nervous system regeneration显示文摘Activation of nuclear factor kappa B(NF-κB) is a hallmark of various central nervous system(CNS) pathologies. Neuron-specific inhibition of its transcriptional activator subunit RelA, also referred to as p65, promotes neuronal survival under a range of conditions, i.e., for ischemic or excitotoxic insults. In macro- and microglial cells, post-lesional activation of NF-κB triggers a growth-permissive program which contributes to neural tissue inflammation, scar formation, and the expression of axonal growth inhibitors. Intriguingly, inhibition of such inducible NF-κB in the neuro-glial compartment, i.e., by genetic ablation of RelA or overexpression of a transdominant negative mutant of its upstream regulator IκBα, significantly enhances functional recovery and promotes axonal regeneration in the mature CNS. By contrast, depletion of the NF-κB subunit p50, which lacks transcriptional activator function and acts as a transcriptional repressor on its own, causes precocious neuronal loss and exacerbates axonal degeneration in the lesioned brain. Collectively, the data imply that NF-κB orchestrates a multicellular program in which κB-dependent gene expression establishes a growth-repulsive terrain within the post-lesioned brain that limits structural regeneration of neuronal circuits. Considering these subunit-specific functions, interference with the NF-κB pathway might hold clinical potentials to improve functional restoration following traumatic CNS injury. | Christian Engelmann Falk Weih Ronny Haenold | 2014 | Neural Regeneration Research2014，9，7： | 8 |
| 2 | Proactive process-level live migration and back migration in HPC environments 显示文摘 | Chao Wang Frank Mueller Christian Engelmann | 2011 | Journal of Parallel and Distributed Computing2011，72，2： | 1 |
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