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Context Info
Confidence 0.45
First Reported 1993
Last Reported 2008
Negated 0
Speculated 1
Reported most in Abstract
Documents 2
Total Number 3
Disease Relevance 1.17
Pain Relevance 2.81

This is a graph with borders and nodes. Maybe there is an Imagemap used so the nodes may be linking to some Pages.

cytosol (Prkcg) plasma membrane (Prkcg) nucleus (Prkcg)
intracellular (Prkcg) response to stress (Prkcg) cytoplasm (Prkcg)
Anatomy Link Frequency
sensory neurons 2
spinal cord 2
nucleus 2
Prkcg (Rattus norvegicus)
Pain Link Frequency Relevance Heat
Kinase C 27 100.00 Very High Very High Very High
nMDA receptor 3 100.00 Very High Very High Very High
Glutamate 3 99.60 Very High Very High Very High
Spinal cord 11 99.12 Very High Very High Very High
substance P 4 98.28 Very High Very High Very High
Calcitonin gene-related peptide 4 97.44 Very High Very High Very High
Sciatic nerve 7 93.84 High High
antagonist 2 86.36 High High
Spontaneous pain 3 76.76 Quite High
Pain 3 75.00 Quite High
Disease Link Frequency Relevance Heat
Nervous System Injury 11 98.98 Very High Very High Very High
Pain 3 76.76 Quite High
Diabetic Nephropathy 3 75.00 Quite High
Hyperalgesia 4 74.32 Quite High
Nociception 2 68.32 Quite High
Disease 1 36.52 Quite Low

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
Consistent with behavioral changes, CCI rats examined 3 or 10 days after sciatic nerve ligation displayed a three-dimensional pattern of increased membrane-bound PKC in the lumbar spinal cord (L1-L5) strikingly different from that of sham-operated rats: in the dorsoventral dimension, reliable increases in membrane-bound PKC occurred mainly within spinal cord laminae I-IV and V-VI in CCI rats; in the ipsilateral-contralateral dimension, changes in membrane-bound PKC were seen on both sides of the spinal cord in CCI rats with reliably higher levels of membrane-bound PKC on the side ipsilateral than on the side contralateral to sciatic nerve ligation; in the rostrocaudal dimension, increases in membrane-bound PKC in the spinal cord dorsal horns of CCI rats extended from spinal segments L2-L5. 4.
Regulation (seen) of Regulation (changes) of PKC in spinal cord associated with kinase c, nervous system injury, sciatic nerve and spinal cord
1) Confidence 0.45 Published 1993 Journal J. Neurophysiol. Section Abstract Doc Link 8410149 Disease Relevance 1.17 Pain Relevance 1.42
Controlling NMDA receptor function and, thus, excitatory transmitter release via modulation of PKC suggests a novel potential target to contrast glutamate excitotoxicity in this motor nucleus.
Regulation (Controlling) of Regulation (modulation) of PKC in nucleus associated with glutamate, kinase c and nmda receptor
2) Confidence 0.44 Published 2008 Journal Eur. J. Neurosci. Section Abstract Doc Link 18445055 Disease Relevance 0 Pain Relevance 0.84
To determine whether protein kinase C (PKC) mediates release of peptides from sensory neurons, we examined the effects of altering PKC activity on resting and evoked release of substance P (SP) and calcitonin gene-related peptide (CGRP).
Spec (examined) Regulation (effects) of Regulation (altering) of PKC in sensory neurons associated with kinase c, calcitonin gene-related peptide and substance p
3) Confidence 0.27 Published 1996 Journal J. Neurochem. Section Abstract Doc Link 8667028 Disease Relevance 0 Pain Relevance 0.56

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