Neuroprotection from stroke in the absence of MHCI or PirB. - Wikidata - awgldk - TriplyDB

Neuroprotection from stroke in the absence of MHCI or PirB.

Neuroprotection from stroke in the absence of MHCI or PirB.

http://www.wikidata.org/entity/Q35857345

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Major Histocompatibility Complex I Expression by Motor Neurons and Its Implication in Amyotrophic Lateral Sclerosis A Common Language: How Neuroimmunological Cross Talk Regulates Adult Hippocampal Neurogenesis The role of the Rho/ROCK signaling pathway in inhibiting axonal regeneration in the central nervous system Axon regeneration impediment: the role of paired immunoglobulin-like receptor B β2-microglobulin is a systemic pro-aging factor that impairs cognitive function and neurogenesis The membrane-active tri-block copolymer pluronic F-68 profoundly rescues rat hippocampal neurons from oxygen-glucose deprivation-induced death through early inhibition of apoptosis Selective estrogen receptor modulators regulate reactive microglia after penetrating brain injury.Inhibition of PirB Activity by TAT-PEP Improves Mouse Motor Ability and Cognitive Behavior.Protection after stroke: cellular effectors of neurovascular unit integrity.Axon growth inhibition by RhoA/ROCK in the central nervous system.Human NgR-Fc decoy protein via lumbar intrathecal bolus administration enhances recovery from rat spinal cord contusion.Targeted inhibition of the Shroom3-Rho kinase protein-protein interaction circumvents Nogo66 to promote axon outgrowth.Blocking PirB up-regulates spines and functional synapses to unlock visual cortical plasticity and facilitate recovery from amblyopia.Distribution of paired immunoglobulin-like receptor B in the nervous system related to regeneration difficulties after unilateral lumbar spinal cord injury.Genomic analysis of reactive astrogliosis Major histocompatibility complex class I proteins in brain development and plasticity.Developmental Sculpting of Intracortical Circuits by MHC Class I H2-Db and H2-Kb.MHCI requires MEF2 transcription factors to negatively regulate synapse density during development and in disease.Efficient subtractive cloning of genes activated by lipopolysaccharide and interferon γ in primary-cultured cortical cells of newborn mice Cell-Autonomous Regulation of Dendritic Spine Density by PirB.Human LilrB2 is a β-amyloid receptor and its murine homolog PirB regulates synaptic plasticity in an Alzheimer's model.Beta-2 microglobulin is important for disease progression in a murine model for amyotrophic lateral sclerosis.A TAP1 null mutation leads to an enlarged olfactory bulb and supernumerary, ectopic olfactory glomeruli.Electroacupuncture enhances rehabilitation through miR-181b targeting PirB after ischemic stroke.Spontaneous ischaemic stroke lesions in a dog brain: neuropathological characterisation and comparison to human ischaemic stroke.PirB is a novel potential therapeutic target for enhancing axonal regeneration and synaptic plasticity following CNS injury in mammals.Astrocytic modulation of blood brain barrier: perspectives on Parkinson's disease.Curcumin prevents reperfusion injury following ischemic stroke in rats via inhibition of NF‑κB, ICAM-1, MMP-9 and caspase-3 expression.Novel Approaches in Astrocyte Protection: from Experimental Methods to Computational Approaches.Mechanisms of Axonal Damage and Repair after Central Nervous System Injury.Relationship Between Obesity, Alzheimer's Disease, and Parkinson's Disease: an Astrocentric View.The Involvement of the Myelin-Associated Inhibitors and Their Receptors in CNS Plasticity and Injury.Synapse elimination and learning rules co-regulated by MHC class I H2-Db.CNS-wide Sexually Dimorphic Induction of the Major Histocompatibility Complex 1 Pathway With Aging.Facial Nerve Recovery in KbDb and C1q Knockout Mice: A Role for Histocompatibility Complex 1 Non-Invasive Monitoring of CNS MHC-I Molecules in Ischemic Stroke Mice.Combination of early constraint-induced movement therapy and fasudil enhances motor recovery after ischemic stroke in rats.The effects of immune protein CD3ζ development and degeneration of retinal neurons after optic nerve injury.MHCI promotes developmental synapse elimination and aging-related synapse loss at the vertebrate neuromuscular junction.Spatio-temporal expression of paired immunoglobulin-like receptor-B in the adult mouse brain after focal cerebral ischaemia.

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Neuroprotection from stroke in the absence of MHCI or PirB.

http://www.wikidata.org/entity/Q35857345

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2012 nî lūn-bûn

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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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2012年论文

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2012年论文

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2012年论文

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name

Neuroprotection from stroke in the absence of MHCI or PirB.

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Neuroprotection from stroke in the absence of MHCI or PirB.

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Neuroprotection from stroke in the absence of MHCI or PirB.

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Neuroprotection from stroke in the absence of MHCI or PirB.

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Neuroprotection from stroke in the absence of MHCI or PirB.

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Neuroprotection from stroke in the absence of MHCI or PirB.

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J.NEURON.2012.01.020

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P1476

Neuroprotection from stroke in the absence of MHCI or PirB

@en

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Barbara K Brott

http://www.w3.org/2001/XMLSchema#string

Carla J Shatz

http://www.w3.org/2001/XMLSchema#string

Lijun Xu

http://www.w3.org/2001/XMLSchema#string

Maja Djurisic

http://www.w3.org/2001/XMLSchema#string

Taeho Kim

http://www.w3.org/2001/XMLSchema#string

Thorsten Naserke

http://www.w3.org/2001/XMLSchema#string

Yi-Bing Ouyang

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P2860

Myelin suppresses axon regeneration by PIR-B/SHP-mediated inhibition of Trk activity

Functional requirement for class I MHC in CNS development and plasticity

CD38 exacerbates focal cytokine production, postischemic inflammation and brain injury after focal cerebral ischemia

Axonal plasticity and functional recovery after spinal cord injury in mice deficient in both glial fibrillary acidic protein and vimentin genes.

Experience-driven plasticity of visual cortex limited by myelin and Nogo receptor

Control of synaptic strength by glial TNFalpha

Strengthening of lateral activation in adult rat visual cortex after retinal lesions captured with voltage-sensitive dye imaging in vivo.

MHC superfamily structure and the immune system.

A potential role for shed soluble major histocompatibility class I molecules as modulators of neurite outgrowth.

The brain-derived neurotrophic factor enhances synthesis of Arc in synaptoneurosomes.

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1100-1107

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scholarly article

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10.1016/J.NEURON.2012.01.020

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6

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73

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George E. Barreto

Jaimie D Adelson

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2012-03-21T00:00:00Z

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221974117

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22445338

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3314229

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