Brain fodrin: substrate for calpain I, an endogenous calcium-activated protease.
about
An alpha-mercaptoacrylic acid derivative is a selective nonpeptide cell-permeable calpain inhibitor and is neuroprotective.The pathogenic activation of calpain: a marker and mediator of cellular toxicity and disease statesBlood biomarkers for brain injury: What are we measuring?Inhibition of E2F1/CDK1 pathway attenuates neuronal apoptosis in vitro and confers neuroprotection after spinal cord injury in vivoExtrasynaptic NMDA receptors couple preferentially to excitotoxicity via calpain-mediated cleavage of STEPCR8, a selective and potent CDK inhibitor, provides neuroprotection in experimental traumatic brain injury.Traumatic white matter injury and glial activation: from basic science to clinics.Calpain mediates proteolysis of the voltage-gated sodium channel alpha-subunit.Disruption of the axon initial segment cytoskeleton is a new mechanism for neuronal injury.A panel of neuron-enriched proteins as markers for traumatic brain injury in humans.The dual role of calcium as messenger and stressor in cell damage, death, and survival.Downregulation of miR-23a and miR-27a following experimental traumatic brain injury induces neuronal cell death through activation of proapoptotic Bcl-2 proteins.Calpain-dependent proteolysis of NF2 protein: involvement in schwannomas and meningiomas.Microwave & magnetic (M2) proteomics reveals CNS-specific protein expression waves that precede clinical symptoms of experimental autoimmune encephalomyelitis.Inhibition of TRPC6 degradation suppresses ischemic brain damage in rats.A pharmacological analysis of the neuroprotective efficacy of the brain- and cell-permeable calpain inhibitor MDL-28170 in the mouse controlled cortical impact traumatic brain injury model.The ankyrin repeat-rich membrane spanning (ARMS)/Kidins220 scaffold protein is regulated by activity-dependent calpain proteolysis and modulates synaptic plasticity.Axonal degeneration in multiple sclerosis: can we predict and prevent permanent disability?Neurodegeneration in glaucoma: progression and calcium-dependent intracellular mechanisms.The biochemistry of memory: The 26year journey of a 'new and specific hypothesis'.Screening an expression library with a ligand probe: isolation and sequence of a cDNA corresponding to a brain calmodulin-binding proteinCalpain activation by Wingless-type murine mammary tumor virus integration site family, member 5A (Wnt5a) promotes axonal growth.Fodrin in centrosomes: implication of a role of fodrin in the transport of gamma-tubulin complex in brain.Increased concentration of spectrin is observed in avian dystrophic muscle.Calpain-mediated processing of p53-associated parkin-like cytoplasmic protein (PARC) affects chemosensitivity of human ovarian cancer cells by promoting p53 subcellular trafficking.Altered autoantigen structure in Sjögren's syndrome: implications for the pathogenesis of autoimmune tissue damage.Selective CDK inhibitor limits neuroinflammation and progressive neurodegeneration after brain trauma.CRYβA3/A1-Crystallin Knockout Develops Nuclear Cataract and Causes Impaired Lysosomal Cargo Clearance and Calpain Activation.Caspase-3- and calpain-mediated tau cleavage are differentially prevented by estrogen and testosterone in beta-amyloid-treated hippocampal neurons.Serum SNTF Increases in Concussed Professional Ice Hockey Players and Relates to the Severity of Postconcussion Symptoms.Voluntary Exercise Preconditioning Activates Multiple Antiapoptotic Mechanisms and Improves Neurological Recovery after Experimental Traumatic Brain Injury.Delayed cell cycle pathway modulation facilitates recovery after spinal cord injuryCurrent status of fluid biomarkers in mild traumatic brain injuryInhibition of calpains improves memory and synaptic transmission in a mouse model of Alzheimer disease.Is the amyloid hypothesis of Alzheimer's disease therapeutically relevant?Calpain-mediated signaling mechanisms in neuronal injury and neurodegenerationNMDA receptor activation and calpain contribute to disruption of dendritic spines by the stress neuropeptide CRH.Evidence That the Blood Biomarker SNTF Predicts Brain Imaging Changes and Persistent Cognitive Dysfunction in Mild TBI PatientsBiochemical, structural, and biomarker evidence for calpain-mediated cytoskeletal change after diffuse brain injury uncomplicated by contusion.Effects of paraquat-induced oxidative stress on the neuronal plasma membrane Ca(2+)-ATPase.
P2860
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P2860
Brain fodrin: substrate for calpain I, an endogenous calcium-activated protease.
description
1984 nî lūn-bûn
@nan
1984年の論文
@ja
1984年学术文章
@wuu
1984年学术文章
@zh-cn
1984年学术文章
@zh-hans
1984年学术文章
@zh-my
1984年学术文章
@zh-sg
1984年學術文章
@yue
1984年學術文章
@zh
1984年學術文章
@zh-hant
name
Brain fodrin: substrate for calpain I, an endogenous calcium-activated protease.
@ast
Brain fodrin: substrate for calpain I, an endogenous calcium-activated protease.
@en
type
label
Brain fodrin: substrate for calpain I, an endogenous calcium-activated protease.
@ast
Brain fodrin: substrate for calpain I, an endogenous calcium-activated protease.
@en
prefLabel
Brain fodrin: substrate for calpain I, an endogenous calcium-activated protease.
@ast
Brain fodrin: substrate for calpain I, an endogenous calcium-activated protease.
@en
P2093
P2860
P356
P1476
Brain fodrin: substrate for calpain I, an endogenous calcium-activated protease.
@en
P2093
P2860
P304
P356
10.1073/PNAS.81.11.3572
P407
P577
1984-06-01T00:00:00Z