INT71244

From wiki-pain
Jump to: navigation, search
Context Info
Confidence 0.30
First Reported 1997
Last Reported 2010
Negated 0
Speculated 0
Reported most in Abstract
Documents 8
Total Number 8
Disease Relevance 2.64
Pain Relevance 4.96

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

cytosol (Prkaca) nucleoplasm (Prkaca) mitochondrion (Prkaca)
Golgi apparatus (Prkaca) plasma membrane (Prkaca) nucleus (Prkaca)
Anatomy Link Frequency
cerebral cortex 2
PGE2 1
Prkaca (Rattus norvegicus)
Pain Link Frequency Relevance Heat
Kinase C 15 100.00 Very High Very High Very High
nMDA receptor 92 99.72 Very High Very High Very High
ketamine 94 99.30 Very High Very High Very High
cerebral cortex 6 98.44 Very High Very High Very High
Hyperalgesia 19 98.00 Very High Very High Very High
Pain 145 97.60 Very High Very High Very High
Neuropathic pain 54 96.76 Very High Very High Very High
dexamethasone 1 96.08 Very High Very High Very High
Spinal nerve ligature 57 95.76 Very High Very High Very High
anesthesia 14 95.16 Very High Very High Very High
Disease Link Frequency Relevance Heat
Hyperalgesia 20 98.00 Very High Very High Very High
Pain 146 97.60 Very High Very High Very High
Neuropathic Pain 84 96.76 Very High Very High Very High
Ganglion Cysts 3 88.20 High High
Arthritis 126 85.60 High High
Nociception 14 71.84 Quite High
Targeted Disruption 1 71.52 Quite High
INFLAMMATION 4 61.64 Quite High
Nervous System Injury 4 61.00 Quite High
Propionic Acidemia 2 57.68 Quite High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
Investigating the interaction between PKC and PKA revealed that although inhibitors of PKA had little effect on PKC-induced modulation of TTX-R INa, inhibitors of PKC significantly attenuated PKA-induced modulation of the current.
PKA Binding (interaction) of associated with kinase c
1) Confidence 0.30 Published 1998 Journal J. Neurosci. Section Abstract Doc Link 9852572 Disease Relevance 0.07 Pain Relevance 0.55
A selective membrane-permeable PKA inhibitor (KT5720) that binds to the catalytic subunits of the cAMP dependent PKA was used [17,50,60].
PKA Binding (binds) of
2) Confidence 0.26 Published 2008 Journal Mol Pain Section Body Doc Link PMC2490682 Disease Relevance 0.42 Pain Relevance 0.60
KT5720 is a widely used selective PKA inhibitor (at nanomolar to low micromolar concentrations) that binds to the catalytic subunits of PKA, causing the displacement of the regulatory subunit and thereby inhibiting the phosphorylating activity of the kinase [50,60]. cAMPS-Rp is a competitive antagonist of cAMP-induced activation of PKA (selective in the low to mid micromolar range) by interacting with cAMP binding sites on the regulatory subunits to prevent cAMP-induced dissociation and activation of the enzyme [51].
PKA Binding (binds) of associated with antagonist
3) Confidence 0.19 Published 2008 Journal Mol Pain Section Body Doc Link PMC2490682 Disease Relevance 0.20 Pain Relevance 0.60
Taken together, these results suggest that MMA, at the same concentrations found in tissues of methylmalonic acidemic children, inhibits the in vitro activities of PKA, CaMKII and PP1 associated with the cytoskeletal fraction of the cerebral cortex of rats, a fact that may be involved with the pathogenesis of the neurological dysfunction characteristic of methylmalonic acidemia.
PKA Binding (associated) of in cerebral cortex associated with anesthesia and cerebral cortex
4) Confidence 0.18 Published 1997 Journal Brain Res. Section Abstract Doc Link 9296563 Disease Relevance 0 Pain Relevance 0.24
Taken together, these results demonstrate that PA inhibits the in vitro activities of PKA, CaMKII, and PP1 associated with the cytoskeletal fraction of the cerebral cortex of rats.
PKA Binding (associated) of in cerebral cortex associated with cerebral cortex
5) Confidence 0.17 Published 1997 Journal Exp. Neurol. Section Abstract Doc Link 9344549 Disease Relevance 0.06 Pain Relevance 0.17
We then tested whether the effect of NO depended on interaction with the adenylyl cyclase-protein kinase A (PKA) pathway, which is known to mediate PGE2-induced hyperalgesia.
PKA Binding (interaction) of in PGE2 associated with hyperalgesia
6) Confidence 0.11 Published 1998 Journal J. Neurosci. Section Abstract Doc Link 9712669 Disease Relevance 1.15 Pain Relevance 1.10
Dexamethasone (DEX; 1 microM) further enhanced FSK- or PMA-induced proENK mRNA expression, which was not correlated with the activation of AP-1 expression and CREB phosphorylation, suggesting that synergistic interaction of glucocorticoid with PKA or PKC pathway for the regulation of proENK mRNA expression appears to be mediated by other pathways rather than CREB and AP-1 families.
PKA Binding (interaction) of associated with dexamethasone
7) Confidence 0.06 Published 2000 Journal Brain Res. Mol. Brain Res. Section Abstract Doc Link 11113530 Disease Relevance 0 Pain Relevance 0.05
Therefore, it is possible that ketamine blocks NMDA receptor and inhibits intracellular PKA, PKC or signals activity, and then decreases NR1 phosphorylation.
PKA Binding (intracellular) of associated with kinase c, ketamine and nmda receptor
8) Confidence 0.03 Published 2010 Journal Mol Pain Section Body Doc Link PMC2942826 Disease Relevance 0.74 Pain Relevance 1.66

General Comments

This test has worked.

Personal tools
Namespaces

Variants
Actions
Navigation
Toolbox