RISK-1: a novel MAPK homologue in axoplasm that is activated and retrogradely transported after nerve injury.
about
Axon regeneration requires a conserved MAP kinase pathway.Differential proteomics reveals multiple components in retrogradely transported axoplasm after nerve injury.The DLK-1 kinase promotes mRNA stability and local translation in C. elegans synapses and axon regenerationCharacterization and reversal of Doxorubicin-mediated biphasic activation of ERK and persistent excitability in sensory neurons of Aplysia californica.Identification of the role of C/EBP in neurite regeneration following microarray analysis of a L. stagnalis CNS injury model.Doxorubicin attenuates serotonin-induced long-term synaptic facilitation by phosphorylation of p38 mitogen-activated protein kinase.Retrograde signaling in injured nerve--the axon reaction revisited.Microtubule depolymerization in Caenorhabditis elegans touch receptor neurons reduces gene expression through a p38 MAPK pathwayPathways that elicit long-term changes in gene expression in nociceptive neurons following nerve injury: contributions to neuropathic pain.Sunday Driver links axonal transport to damage signaling.Effects of axotomy on cultured sensory neurons of Aplysia: long-term injury-induced changes in excitability and morphology are mediated by different signaling pathways.Cellular, molecular, and epigenetic mechanisms in non-associative conditioning: implications for pain and memoryThe role of local protein synthesis and degradation in axon regenerationRole of transcription factors in peripheral nerve regeneration.Remote neurodegeneration: multiple actors for one play.Gene expression profiling of experimental traumatic spinal cord injury as a function of distance from impact site and injury severity.Synaptic generation of an intracellular retrograde signal requires activation of the tyrosine kinase and mitogen-activated protein kinase signaling cascades in AplysiaBorrelia burgdorferi-induced expression of matrix metalloproteinases from human chondrocytes requires mitogen-activated protein kinase and Janus kinase/signal transducer and activator of transcription signaling pathways.Injury-induced decline of intrinsic regenerative ability revealed by quantitative proteomics.Evidence that long-term hyperexcitability of the sensory neuron soma induced by nerve injury in Aplysia is adaptive.Serotonin induces memory-like, rapamycin-sensitive hyperexcitability in sensory axons of aplysia that contributes to injury responses.
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RISK-1: a novel MAPK homologue in axoplasm that is activated and retrogradely transported after nerve injury.
description
2001 nî lūn-bûn
@nan
2001年の論文
@ja
2001年学术文章
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2001年学术文章
@zh
2001年学术文章
@zh-cn
2001年学术文章
@zh-hans
2001年学术文章
@zh-my
2001年学术文章
@zh-sg
2001年學術文章
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2001年學術文章
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name
RISK-1: a novel MAPK homologue ...... ransported after nerve injury.
@en
RISK-1: a novel MAPK homologue ...... ransported after nerve injury.
@nl
type
label
RISK-1: a novel MAPK homologue ...... ransported after nerve injury.
@en
RISK-1: a novel MAPK homologue ...... ransported after nerve injury.
@nl
prefLabel
RISK-1: a novel MAPK homologue ...... ransported after nerve injury.
@en
RISK-1: a novel MAPK homologue ...... ransported after nerve injury.
@nl
P2093
P2860
P356
P1476
RISK-1: a novel MAPK homologue ...... ransported after nerve injury.
@en
P2093
P2860
P356
10.1002/NEU.1016
P577
2001-04-01T00:00:00Z