INT48959

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Context Info
Confidence 0.70
First Reported 1993
Last Reported 2010
Negated 3
Speculated 8
Reported most in Abstract
Documents 52
Total Number 60
Disease Relevance 16.47
Pain Relevance 36.49

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
spinal 9
neurons 8
spinal cord 6
spinal cord dorsal horns 5
aorta 2
Prkcg (Rattus norvegicus)
Pain Link Frequency Relevance Heat
Kinase C 582 100.00 Very High Very High Very High
Spinal cord 246 100.00 Very High Very High Very High
nav1.8 67 100.00 Very High Very High Very High
COX2 5 100.00 Very High Very High Very High
excitatory amino acid 4 100.00 Very High Very High Very High
substance P 240 99.98 Very High Very High Very High
tolerance 223 99.96 Very High Very High Very High
Nerve growth factor 31 99.92 Very High Very High Very High
Calcium channel 5 99.90 Very High Very High Very High
qutenza 143 99.70 Very High Very High Very High
Disease Link Frequency Relevance Heat
Nervous System Injury 47 100.00 Very High Very High Very High
Adult Respiratory Distress Syndrome 26 100.00 Very High Very High Very High
Hypoxia 29 99.98 Very High Very High Very High
Ganglion Cysts 240 99.76 Very High Very High Very High
Drug Induced Neurotoxicity 7 99.70 Very High Very High Very High
Hyperglycemia 3 99.60 Very High Very High Very High
Diabetes Mellitus 44 99.48 Very High Very High Very High
Hyperalgesia 102 99.38 Very High Very High Very High
Cv General 4 Under Development 15 99.12 Very High Very High Very High
INFLAMMATION 145 98.76 Very High Very High Very High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
In addition, intracellular perfusion with 5 mM bis-(o-aminophenoxy)-N,N,N',N'-tetraacetic acid (BAPTA) or pretreatment with omega-conotoxin GVIA or Cd(2+)-Ringer, but not nifedipine, prevented the PDBu-induced suppression of I(K) at -50 mV, suggesting that a voltage-dependent influx of calcium through N-type calcium channels was necessary for the activation of PKC.
Positive_regulation (necessary) of Positive_regulation (activation) of PKC associated with kinase c, calcium channel and conotoxin
1) Confidence 0.70 Published 2001 Journal J. Neurophysiol. Section Abstract Doc Link 11152736 Disease Relevance 0 Pain Relevance 0.43
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.
Positive_regulation (extended) of in spinal Positive_regulation (increases) of PKC in spinal cord dorsal horns associated with kinase c, nervous system injury, sciatic nerve and spinal cord
2) Confidence 0.50 Published 1993 Journal J. Neurophysiol. Section Abstract Doc Link 8410149 Disease Relevance 1.06 Pain Relevance 1.39
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.
Positive_regulation (occurred) of Positive_regulation (increases) of PKC in spinal cord associated with kinase c, nervous system injury, sciatic nerve and spinal cord
3) Confidence 0.50 Published 1993 Journal J. Neurophysiol. Section Abstract Doc Link 8410149 Disease Relevance 1.15 Pain Relevance 1.41
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.
Positive_regulation (increases) of Positive_regulation (increases) of PKC in spinal cord dorsal horns associated with kinase c, nervous system injury, sciatic nerve and spinal cord
4) Confidence 0.50 Published 1993 Journal J. Neurophysiol. Section Abstract Doc Link 8410149 Disease Relevance 0.99 Pain Relevance 1.34
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.
Positive_regulation (increases) of Positive_regulation (increases) of PKC in spinal cord associated with kinase c, nervous system injury, sciatic nerve and spinal cord
5) Confidence 0.50 Published 1993 Journal J. Neurophysiol. Section Abstract Doc Link 8410149 Disease Relevance 1.10 Pain Relevance 1.41
We report here that the current and voltage responses activated by capsaicin were markedly increased by phorbol 12-myristate 13-acetate (PMA), an activator of protein kinase C (PKC).
Positive_regulation (increased) of Positive_regulation (activator) of PKC associated with kinase c and qutenza
6) Confidence 0.50 Published 2001 Journal Neuropharmacology Section Abstract Doc Link 11587715 Disease Relevance 0.35 Pain Relevance 0.76
This suggests that PKC activation potentiates but does not solely mediate lindane's inhibitory action on gap junctional communication.
Neg (not) Positive_regulation (mediate) of Positive_regulation (activation) of PKC associated with kinase c
7) Confidence 0.49 Published 1995 Journal Toxicol. Appl. Pharmacol. Section Abstract Doc Link 7532876 Disease Relevance 0 Pain Relevance 0.31
These results suggest that activation of PKC can augment the release of peptides in the spinal cord, which could increase nociceptive sensory transmission and contribute to hyperalgesia.
Positive_regulation (augment) of Positive_regulation (activation) of PKC in spinal cord associated with nociception, hyperalgesia, kinase c and spinal cord
8) Confidence 0.49 Published 1999 Journal Neurosci. Lett. Section Abstract Doc Link 10327195 Disease Relevance 0.32 Pain Relevance 0.89
Using both extracellular field potential and whole-cell patch-clamp recordings in brainstem parasagital slices of juvenile rat with the mandibular nerve attached, we show here that the induction of trigeminal primary afferent LTP: (1) does not require the activation of ionotropic glutamate receptors; (2) is dependent on extracellular Ca(2+) and the release of Ca(2+) from intracellular stores; (3) is specifically prevented by the metabotropic glutamate receptor subtype 5 (mGluR5) antagonist 2-methyl-6-(phenylethynyl)pyridine but not the mGluR1 antagonist LY367385, group II mGluR antagonist LY341495 or group III mGluR antagonist MAP4; (4) is mimicked by the bath-applied group I mGluR agonist (S)-3,5-dihydroxyphenylglycine and mGluR5 agonist (RS)-2-chloro-5-hydroxyphenylglycine; (5) requires the activation of phospholipase C (PLC) and protein kinase C (PKC); and (6) is concomitantly with a decrease in paired-pulse depression.
Positive_regulation (requires) of Positive_regulation (activation) of PKC in juvenile associated with medulla, kinase c, depression, antagonist, glutamate receptor, agonist and long-term potentiation
9) Confidence 0.49 Published 2005 Journal Pain Section Abstract Doc Link 15777867 Disease Relevance 0.10 Pain Relevance 0.87
Protein kinase C (PKC) activation by phorbol-12-myristate-13-acetate (PMA) increased the hyposmolarity-elicited exocytosis and this activation increased glutamate (80%), GABA (51%) and taurine (42%) hyposmotic efflux.
Positive_regulation (increased) of Positive_regulation (activation) of PKC associated with gaba, glutamate and kinase c
10) Confidence 0.49 Published 2004 Journal Eur. J. Neurosci. Section Abstract Doc Link 15009139 Disease Relevance 0.10 Pain Relevance 0.66
Previous studies had indicated that a potential function for PKC?
Positive_regulation (indicated) of Positive_regulation (function) of PKC associated with kinase c
11) Confidence 0.49 Published 2007 Journal Reprod Biol Endocrinol Section Body Doc Link PMC2041951 Disease Relevance 0 Pain Relevance 0.31
Renal pelvic perfusion with 4beta-phorbol 12,13-dibutyrate (PDBu) to activate PKC increased ARNA 27 +/- 4% and renal pelvic release of PGE(2) from 500 +/- 59 to 1, 113 +/- 183 pg/min and substance P from 10 +/- 2 to 30 +/- 2 pg/min (all P < 0.01).
Positive_regulation (activate) of Positive_regulation (increased) of PKC associated with kinase c and substance p
12) Confidence 0.48 Published 2000 Journal Am. J. Physiol. Regul. Integr. Comp. Physiol. Section Abstract Doc Link 10749782 Disease Relevance 0 Pain Relevance 0.92
Protein kinase C (PKC) activation increases ARNA, and PKC inhibition blocks the ARNA response to bradykinin.
Positive_regulation (increases) of Positive_regulation (activation) of PKC associated with kinase c and bradykinin
13) Confidence 0.48 Published 2000 Journal Am. J. Physiol. Regul. Integr. Comp. Physiol. Section Abstract Doc Link 10749782 Disease Relevance 0 Pain Relevance 0.64
Spinal activation of PKC increases release of glutamate in vivo [9] and in vitro [12], and formalin-induced release of glutamate is prevented by blockade of PKC [17].
Positive_regulation (increases) of Positive_regulation (activation) of PKC in Spinal associated with glutamate and kinase c
14) Confidence 0.48 Published 2006 Journal Mol Pain Section Body Doc Link PMC1482680 Disease Relevance 0 Pain Relevance 1.33
Thus, omega-CgTx (N-type Ca channels) may regulate neurotransmitter release evoked by C fiber activation and the formalin-evoked hyperalgesia may possibly be provoked as a result of PKC activation elicited by both presynaptic neurotransmitter release and activation of NMDA receptors in the spinal neurons.
Positive_regulation (result) of Positive_regulation (activation) of PKC in spinal associated with c fibre, hyperalgesia, neurotransmitter and nmda receptor
15) Confidence 0.47 Published 1999 Journal Cell. Mol. Neurobiol. Section Abstract Doc Link 10081603 Disease Relevance 0.17 Pain Relevance 0.68
Activation of protein kinase C (PKC) by 3,4-methylenedioxymethamphetamine (MDMA) occurs through the stimulation of serotonin receptors and transporter.
Positive_regulation (occurs) of Positive_regulation (Activation) of PKC associated with kinase c and serotonin
16) Confidence 0.47 Published 1997 Journal Neuropsychopharmacology Section Title Doc Link 9272479 Disease Relevance 0 Pain Relevance 0.40
In our previous studies, we found that intrathecal (i.t.) injection of pertussis toxin (PTX) produces thermal hyperalgesia, which is poorly responsive to morphine and is accompanied by an increase in cerebrospinal fluid (CSF) levels of excitatory amino acids (EAAs) and protein kinase C (PKC) activation.
Positive_regulation (increase) of Positive_regulation (increase) of PKC in CSF associated with kinase c, bordatella infection, thermal hyperalgesia, excitatory amino acid, morphine and intrathecal
17) Confidence 0.47 Published 2006 Journal Life Sci. Section Abstract Doc Link 16271370 Disease Relevance 0.45 Pain Relevance 1.22
These results suggest that the 8-Br-cAMP-induced increase in Nav 1.8 currents may be mediated by activation of both PKA and PKC.
Spec (may) Positive_regulation (mediated) of Positive_regulation (activation) of PKC associated with kinase c
18) Confidence 0.46 Published 2007 Journal Neuropharmacology Section Abstract Doc Link 17140607 Disease Relevance 0.07 Pain Relevance 0.24
We examined whether 8-bromo-cAMP (8-Br-cAMP)-induced modification of tetrodotoxin-resistant (TTX-R) sodium current in neonatal rat nodose ganglion neurons is mediated by the activation of protein kinase A (PKA) and/or protein kinase C (PKC).
Positive_regulation (mediated) of Positive_regulation (activation) of PKC in neurons associated with ganglion cysts, tetrodotoxin and kinase c
19) Confidence 0.46 Published 2007 Journal Neuropharmacology Section Abstract Doc Link 17140607 Disease Relevance 0.17 Pain Relevance 0.43
Activation of either PKC or PKA increased TTX-R INa.
Positive_regulation (increased) of Positive_regulation (Activation) of PKC associated with kinase c
20) Confidence 0.46 Published 1998 Journal J. Neurosci. Section Abstract Doc Link 9852572 Disease Relevance 0.09 Pain Relevance 0.41

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