PAR-1 deficiency protects against neuronal damage and neurologic deficits after unilateral cerebral hypoxia/ischemia.
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The Importance of Thrombin in Cerebral Injury and DiseaseSerine proteases, serine protease inhibitors, and protease-activated receptors: roles in synaptic function and behaviorLearning and memory deficits in mice lacking protease activated receptor-1.Protease-activated receptor-1 activation by granzyme B causes neurotoxicity that is augmented by interleukin-1βDeficiency of PAR4 attenuates cerebral ischemia/reperfusion injury in miceGranzyme B-induced neurotoxicity is mediated via activation of PAR-1 receptor and Kv1.3 channel.PAR1-activated astrocytes in the nucleus of the solitary tract stimulate adjacent neurons via NMDA receptors.Thrombin activity associated with neuronal damage during acute focal ischemiaStratification substantially reduces behavioral variability in the hypoxic-ischemic stroke model.Contribution of protease-activated receptor 1 in status epilepticus-induced epileptogenesis.Protease-activated receptor-1 modulates hippocampal memory formation and synaptic plasticityBaicalin protects against thrombin induced cell injury in SH-SY5Y cellsProtease-activated receptor 1-dependent neuronal damage involves NMDA receptor function.A protease-activated receptor 1 antagonist protects against global cerebral ischemia/reperfusion injury after asphyxial cardiac arrest in rabbits.Activation of protease activated receptor 1 increases the excitability of the dentate granule neurons of hippocampusTargeting the thrombin receptor modulates inflammation and astrogliosis to improve recovery after spinal cord injuryInhibition of Protease-Activated Receptor 1 Does not Affect Dendritic Homeostasis of Cultured Mouse Dentate Granule Cells.Role of protease-activated receptor-1 in brain injury after experimental global cerebral ischemia.PAR-1 antagonist SCH79797 ameliorates apoptosis following surgical brain injury through inhibition of ASK1-JNK in rats.Plasmin Activation of Glial Cells through Protease-Activated Receptor 1.Baicalin attenuates focal cerebral ischemic reperfusion injury by inhibition of protease-activated receptor-1 and apoptosis.Reduction of intracerebral hemorrhage by rivaroxaban after tPA thrombolysis is associated with downregulation of PAR-1 and PAR-2.
P2860
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P2860
PAR-1 deficiency protects against neuronal damage and neurologic deficits after unilateral cerebral hypoxia/ischemia.
description
2004 nî lūn-bûn
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2004年の論文
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2004年学术文章
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2004年学术文章
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2004年学术文章
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2004年学术文章
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2004年学术文章
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2004年學術文章
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name
PAR-1 deficiency protects agai ...... ral cerebral hypoxia/ischemia.
@en
PAR-1 deficiency protects agai ...... ral cerebral hypoxia/ischemia.
@nl
type
label
PAR-1 deficiency protects agai ...... ral cerebral hypoxia/ischemia.
@en
PAR-1 deficiency protects agai ...... ral cerebral hypoxia/ischemia.
@nl
prefLabel
PAR-1 deficiency protects agai ...... ral cerebral hypoxia/ischemia.
@en
PAR-1 deficiency protects agai ...... ral cerebral hypoxia/ischemia.
@nl
P2093
P2860
P1476
PAR-1 deficiency protects agai ...... ral cerebral hypoxia/ischemia.
@en
P2093
Ellen E Olson
Polina Lyuboslavsky
Robert J McKeon
Stephen F Traynelis
P2860
P304
P356
10.1097/01.WCB.0000128266.87474.BF
P577
2004-09-01T00:00:00Z
P5875
P6179
1043105588