Thrombin signaling in the brain: the role of protease-activated receptors.
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The Importance of Thrombin in Cerebral Injury and DiseaseInsights into the physiological function of the β-amyloid precursor protein: beyond Alzheimer's diseaseIntercellular cross-talk in intracerebral hemorrhageProteinase-activated receptor-1 and -2 induce the release of chemokine GRO/CINC-1 from rat astrocytes via differential activation of JNK isoforms, evoking multiple protective pathways in brainInternalization and desensitization of a green fluorescent protein-tagged P2Y nucleotide receptor are differently controlled by inhibition of calmodulin-dependent protein kinase II.Nafamostat mesilate attenuates neuronal damage in a rat model of transient focal cerebral ischemia through thrombin inhibition.Protease-activated receptor-1 activation by granzyme B causes neurotoxicity that is augmented by interleukin-1βInhibition of SRC family kinases protects hippocampal neurons and improves cognitive function after traumatic brain injury.Blood-brain barrier breakdown and repair by Src after thrombin-induced injury.Granzyme B-induced neurotoxicity is mediated via activation of PAR-1 receptor and Kv1.3 channel.Matrix metalloproteinases, synaptic injury, and multiple sclerosisThrombin enhances NGF-mediated neurite extension via increased and sustained activation of p44/42 MAPK and p38 MAPK.Fibrinogen inhibits neurite outgrowth via beta 3 integrin-mediated phosphorylation of the EGF receptorSurgery increases cell death and induces changes in gene expression compared with anesthesia alone in the developing piglet brain.Volume transmission and wiring transmission from cellular to molecular networks: history and perspectives.Src kinase inhibition decreases thrombin-induced injury and cell cycle re-entry in striatal neurons.PACAP38 protects rat cortical neurons against the neurotoxicity evoked by sodium nitroprusside and thrombin.The effect of thrombin on a 6-hydroxydopamine model of Parkinson's disease depends on timing.Microarray analysis of prothrombin knockdown in zebrafish.Cell cycle inhibition without disruption of neurogenesis is a strategy for treatment of central nervous system diseases.PG2 for patients with acute spontaneous intracerebral hemorrhage: a double-blind, randomized, placebo-controlled study.The regulation of the CNS innate immune response is vital for the restoration of tissue homeostasis (repair) after acute brain injury: a brief review.The Molecular Mechanisms that Promote Edema After Intracerebral Hemorrhage.Excitatory and Mitogenic Signaling in Cell Death, Blood-brain Barrier Breakdown, and BBB Repair after Intracerebral Hemorrhage.Modulatory Role of Nurr1 Activation and Thrombin Inhibition in the Neuroprotective Effects of Dabigatran Etexilate in Rotenone-Induced Parkinson's Disease in Rats.The involvement of thrombin in the pathogenesis of glioblastoma.Astrocytic control of synaptic NMDA receptors.Homeostatic effects of coagulation protease-dependent signaling and protease activated receptors.Thrombin-promoted release of UDP-glucose from human astrocytoma cells.Activity of recombinant trypsin isoforms on human proteinase-activated receptors (PAR): mesotrypsin cannot activate epithelial PAR-1, -2, but weakly activates brain PAR-1.Proximate Mediators of Microvascular Dysfunction at the Blood-Brain Barrier: Neuroinflammatory Pathways to NeurodegenerationProtease-activated receptor 1 (PAR1) coupling to G(q/11) but not to G(i/o) or G(12/13) is mediated by discrete amino acids within the receptor second intracellular loop.Neuro-Coagulopathy: Blood Coagulation Factors in Central Nervous System Diseases.The microglia-activating potential of thrombin: the protease is not involved in the induction of proinflammatory cytokines and chemokines.Proteinase-activated receptor-1 activation presynaptically enhances spontaneous glutamatergic excitatory transmission in adult rat substantia gelatinosa neurons.Recovery from trauma induced amnesia correlates with normalization of thrombin activity in the mouse hippocampus.Protease-activated receptor-1 protects rat astrocytes from apoptotic cell death via JNK-mediated release of the chemokine GRO/CINC-1.Cell cycle inhibition without disruption of neurogenesis is a strategy for treatment of aberrant cell cycle diseases: an update.Phosphorylation of Ser45 and Ser59 of αB-crystallin and p38/extracellular regulated kinase activity determine αB-crystallin-mediated protection of rat brain astrocytes from C2-ceramide- and staurosporine-induced cell death.
P2860
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P2860
Thrombin signaling in the brain: the role of protease-activated receptors.
description
2003 nî lūn-bûn
@nan
2003 թուականի Փետրուարին հրատարակուած գիտական յօդուած
@hyw
2003 թվականի փետրվարին հրատարակված գիտական հոդված
@hy
2003年の論文
@ja
2003年学术文章
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2003年学术文章
@zh-cn
2003年学术文章
@zh-hans
2003年学术文章
@zh-my
2003年学术文章
@zh-sg
2003年學術文章
@yue
name
Thrombin signaling in the brain: the role of protease-activated receptors.
@ast
Thrombin signaling in the brain: the role of protease-activated receptors.
@en
type
label
Thrombin signaling in the brain: the role of protease-activated receptors.
@ast
Thrombin signaling in the brain: the role of protease-activated receptors.
@en
prefLabel
Thrombin signaling in the brain: the role of protease-activated receptors.
@ast
Thrombin signaling in the brain: the role of protease-activated receptors.
@en
P2860
P356
P1433
P1476
Thrombin signaling in the brain: the role of protease-activated receptors.
@en
P2093
Georg Reiser
P2860
P304
P356
10.1515/BC.2003.021
P577
2003-02-01T00:00:00Z