Cyclin D1 gene ablation confers neuroprotection in traumatic brain injury
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Neuroprotection for traumatic brain injuryGenetic manipulation of cell death and neuroplasticity pathways in traumatic brain injuryUpregulation of SYF2 is associated with neuronal apoptosis caused by reactive astrogliosis to neuroinflammationCR8, a selective and potent CDK inhibitor, provides neuroprotection in experimental traumatic brain injury.What's New in Traumatic Brain Injury: Update on Tracking, Monitoring and TreatmentSelective CDK inhibitors: promising candidates for future clinical traumatic brain injury trials.Delayed mGluR5 activation limits neuroinflammation and neurodegeneration after traumatic brain injury.Bilateral gene interaction hierarchy analysis of the cell death gene response emphasizes the significance of cell cycle genes following unilateral traumatic brain injuryVoluntary Exercise Preconditioning Activates Multiple Antiapoptotic Mechanisms and Improves Neurological Recovery after Experimental Traumatic Brain Injury.Delayed expression of cell cycle proteins contributes to astroglial scar formation and chronic inflammation after rat spinal cord contusionS100B inhibition reduces behavioral and pathologic changes in experimental traumatic brain injury.Ablation of the transcription factors E2F1-2 limits neuroinflammation and associated neurological deficits after contusive spinal cord injuryThe effect of STAT3 inhibition on status epilepticus and subsequent spontaneous seizures in the pilocarpine model of acquired epilepsy.Neurocognitive functioning and genetic variation in patients with primary brain tumours.CR8, a novel inhibitor of CDK, limits microglial activation, astrocytosis, neuronal loss, and neurologic dysfunction after experimental traumatic brain injury.Microglial-derived microparticles mediate neuroinflammation after traumatic brain injury.Traumatic brain injury using mouse models.Upregulation of PRDM5 Is Associated with Astrocyte Proliferation and Neuronal Apoptosis Caused by Lipopolysaccharide.A Compact Blast-Induced Traumatic Brain Injury Model in Mice.Metabolomics and neuroanatomical evaluation of post-mortem changes in the hippocampus.Combined inhibition of cell death induced by apoptosis inducing factor and caspases provides additive neuroprotection in experimental traumatic brain injury.Cell cycle inhibition reduces inflammatory responses, neuronal loss, and cognitive deficits induced by hypobaria exposure following traumatic brain injury.Interferon-Alpha Reduces Human Hippocampal Neurogenesis and Increases Apoptosis via Activation of Distinct STAT1-Dependent Mechanisms.Cyclin D1 is required for proliferation of Olig2-expressing progenitor cells in the injured cerebral cortex.Stage-specific requirement for cyclin D1 in glial progenitor cells of the cerebral cortex.
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Cyclin D1 gene ablation confers neuroprotection in traumatic brain injury
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2012 nî lūn-bûn
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2012年の論文
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2012年論文
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2012年論文
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2012年論文
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name
Cyclin D1 gene ablation confers neuroprotection in traumatic brain injury
@ast
Cyclin D1 gene ablation confers neuroprotection in traumatic brain injury
@en
type
label
Cyclin D1 gene ablation confers neuroprotection in traumatic brain injury
@ast
Cyclin D1 gene ablation confers neuroprotection in traumatic brain injury
@en
prefLabel
Cyclin D1 gene ablation confers neuroprotection in traumatic brain injury
@ast
Cyclin D1 gene ablation confers neuroprotection in traumatic brain injury
@en
P2093
P2860
P50
P356
P1476
Cyclin D1 gene ablation confers neuroprotection in traumatic brain injury
@en
P2093
Alan I Faden
Marie Hanscom
Ming T Tan
Rainier M Cabatbat
Shruti V Kabadi
P2860
P304
P356
10.1089/NEU.2011.1980
P577
2012-01-13T00:00:00Z