INT119400

From wiki-pain
Jump to: navigation, search
Context Info
Confidence 0.52
First Reported 2004
Last Reported 2010
Negated 1
Speculated 0
Reported most in Body
Documents 19
Total Number 19
Disease Relevance 8.47
Pain Relevance 11.63

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

cytosol (Car2) extracellular space (Car2) lyase activity (Car2)
cytoplasm (Car2)
Anatomy Link Frequency
vesicles 1
thalamus 1
hippocampus 1
Car2 (Mus musculus)
Pain Link Frequency Relevance Heat
Kinase C 91 100.00 Very High Very High Very High
Morphine 97 99.82 Very High Very High Very High
withdrawal 43 99.82 Very High Very High Very High
dexamethasone 3 98.76 Very High Very High Very High
cytokine 84 98.74 Very High Very High Very High
Opioid 15 98.24 Very High Very High Very High
tolerance 8 97.96 Very High Very High Very High
Hippocampus 58 97.88 Very High Very High Very High
qutenza 183 97.84 Very High Very High Very High
adenocard 11 97.64 Very High Very High Very High
Disease Link Frequency Relevance Heat
Nociception 128 99.84 Very High Very High Very High
Calcification 59 99.16 Very High Very High Very High
Diabetes Mellitus 67 97.76 Very High Very High Very High
Chronic Renal Failure 3 97.28 Very High Very High Very High
Injury 23 95.60 Very High Very High Very High
Hypersensitivity 5 95.00 High High
INFLAMMATION 109 94.80 High High
Hyperalgesia 26 93.68 High High
Disease 124 91.84 High High
Nervous System Injury 32 91.60 High High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
Interestingly, repeated co-administration of dizocilpine and morphine prevented the withdrawal-induced phosphorylation of Ca2+/calmodulin kinase II (p-CaMK II) in the cortex, but not in the thalamus.
Phosphorylation (phosphorylation) of Ca2 in thalamus associated with thalamus, withdrawal and morphine
1) Confidence 0.52 Published 2004 Journal Behav. Brain Res. Section Abstract Doc Link 15196794 Disease Relevance 0.23 Pain Relevance 1.57
CREB can be activated by both protein kinase A and by Ca2+-calmodulin-dependent protein kinases (CaMKs), which are in turn phosphorylated by their upstream activators CaMKKalpha and CaMMKKbeta.
Phosphorylation (phosphorylated) of Ca2
2) Confidence 0.45 Published 2004 Journal Neuropharmacology Section Abstract Doc Link 15555640 Disease Relevance 0.36 Pain Relevance 0.72
Moreover, because more than one type of Ca2+-acitvated Cl?
Phosphorylation (type) of Ca2
3) Confidence 0.43 Published 2010 Journal The Journal of General Physiology Section Body Doc Link PMC2806418 Disease Relevance 0 Pain Relevance 0
Phosphorylation of neurogranin, protein kinase C, and Ca2+/calmodulin dependent protein kinase II in opioid tolerance and dependence.
Phosphorylation (Phosphorylation) of Ca2 associated with addiction, kinase c, tolerance and opioid
4) Confidence 0.36 Published 2006 Journal Neurosci. Lett. Section Title Doc Link 16824682 Disease Relevance 0 Pain Relevance 1.34
TRPV1 can be sensitized by phosphorylation through PKC, PKA and Ca2+/CaM-dependent kinsase II [17-20].
Phosphorylation (phosphorylation) of Ca2
5) Confidence 0.31 Published 2006 Journal Mol Pain Section Body Doc Link PMC1660571 Disease Relevance 1.31 Pain Relevance 1.13
Despite increases in [Ca2+]i, morphine treatment alone did not increase cytokine release suggesting that an additional signal independent from Ca2+, such as the phosphorylation of NF-?
Phosphorylation (phosphorylation) of Ca2 associated with cytokine and morphine
6) Confidence 0.28 Published 2008 Journal PLoS ONE Section Body Doc Link PMC2605563 Disease Relevance 0 Pain Relevance 0.74
Extracellular signal-regulated kinases (ERKs), major subfamilies of mitogen-activated protein kinases (MAPKs), are phosphorylated following membrane depolarization and Ca2+ influx [15].
Phosphorylation (phosphorylated) of Ca2
7) Confidence 0.28 Published 2008 Journal Mol Pain Section Body Doc Link PMC2599895 Disease Relevance 0.33 Pain Relevance 0.33
Extracellular signal-regulated kinases (ERKs), representing one of the major subfamilies of mitogen-activated protein kinases (MAPKs), are phosphorylated following membrane depolarization and Ca2+ influx [2].
Phosphorylation (phosphorylated) of Ca2
8) Confidence 0.25 Published 2008 Journal Mol Pain Section Body Doc Link PMC2488330 Disease Relevance 1.17 Pain Relevance 0.85
To better understand the role of CREB in opioids dependence and underlying signal pathways, we compared the effects of three ohmfentanyl stereoisomers ((-)-cis-(3R,4S,2'R) OMF (F9202), (+)-cis-(3R,4S,2'S) OMF (F9204), (-)-cis-(3S,4S,2'R) OMF (F9203)) and morphine on CREB phosphorylation and the expression of Ca2+/calmodulin-dependent protein kinase IV (CaMKIV) in hippocampus derived from mice which displayed conditioned place preference (CPP) behavior by Western blot, and immunohistochemistry analyses.
Phosphorylation (phosphorylation) of Ca2 in hippocampus associated with addiction, hippocampus, opioid and morphine
9) Confidence 0.20 Published 2004 Journal Brain Res. Section Abstract Doc Link 15451364 Disease Relevance 0 Pain Relevance 0.60
Thus, Ca2+-mediated dephosphorylation may render the channel inactive leading to desensitization or tachyphylaxis.
Phosphorylation (dephosphorylation) of Ca2
10) Confidence 0.19 Published 2008 Journal Current Neuropharmacology Section Body Doc Link PMC2647151 Disease Relevance 0.45 Pain Relevance 0.91
Increases in intracellular Ca2+ initiate several second messenger pathways including the activation of phospholipase A2 (PLA2), phospholipase C (PLC) and Ca2+-dependent kinases, which can lead to the generation of AA and its metabolites, release of Ca2+ from intracellular stores and phosphorylation of nociceptive ion channels, respectively.
Phosphorylation (phosphorylation) of Ca2 associated with nociception
11) Confidence 0.14 Published 2008 Journal Current Neuropharmacology Section Body Doc Link PMC2647151 Disease Relevance 0.61 Pain Relevance 0.50
Calmodulin is likely to regulate binding of dystrophin/utrophin to actin [87], while the Ca2+/calmodulin dependent kinase, CaMKII, actively phosphorylates both dystrophin and syntrophin [88].
Phosphorylation (phosphorylates) of Ca2
12) Confidence 0.13 Published 2009 Journal Mol Neurobiol Section Body Doc Link PMC2840664 Disease Relevance 0.33 Pain Relevance 0.04
Increases in intracellular Ca2+ initiate several second messenger pathways, including activation of PLA2, PLC and Ca2+-dependent kinases, which can lead to the generation of AA and its metabolites, release of Ca2+ from intracellular stores, and phosphorylation of nociceptive receptors, respectively.
Phosphorylation (phosphorylation) of Ca2 associated with nociception
13) Confidence 0.13 Published 2006 Journal Mol Pain Section Body Doc Link PMC1563450 Disease Relevance 0.83 Pain Relevance 1.09
In contrast, Tian et al. suggested that the increase in the slow after-hyperpolarization amplitude seen after exposure to high doses of corticosterone may involve cAMP-dependent phosphorylation and Ca2+-activated K+ channels [102]: dexamethasone (1 ?
Phosphorylation (phosphorylation) of Ca2 associated with dexamethasone
14) Confidence 0.10 Published 2010 Journal Mol Brain Section Body Doc Link PMC2841592 Disease Relevance 0.06 Pain Relevance 0.42
Increases in intracellular Ca2+ initiate several second messenger pathways, including activation of PLA2, PLC and Ca2+-dependent kinases, which can lead to the generation of AA and its metabolites, release of Ca2+ from intracellular stores, and phosphorylation of nociceptive receptors, respectively.
Phosphorylation (phosphorylation) of Ca2 associated with nociception
15) Confidence 0.10 Published 2006 Journal Mol Pain Section Body Doc Link PMC1563450 Disease Relevance 0.79 Pain Relevance 0.97
Another recent study does not entirely support the hypothesis on the role of PP-1, as they have some evidence that CaMK-II modulation of GABAA receptors critically requires Ca2+/CaM binding to CaMK-II but not autophosphorylation (C.
Neg (not) Phosphorylation (autophosphorylation) of Ca2
16) Confidence 0.09 Published 2008 Journal Frontiers in Molecular Neuroscience Section Body Doc Link PMC2526003 Disease Relevance 0 Pain Relevance 0.08
This triggers a rise in the concentration of Ca2+ in the cells and the subsequent activation (together with DAG) of protein kinase C (PKC) and finally the release of pre-synthesised insulin, which is stored in secretory vesicles.
Phosphorylation (concentration) of Ca2 in vesicles associated with kinase c
17) Confidence 0.09 Published 2010 Journal The Open Biochemistry Journal Section Body Doc Link PMC2864432 Disease Relevance 0 Pain Relevance 0.18
The permeability of the connexons can be regulated through many mechanisms including changes in [Ca2+], pH and phosphorylation by several protein kinases [258,259], including PKC?
Phosphorylation (phosphorylation) of Ca2 associated with kinase c
18) Confidence 0.07 Published 2007 Journal Biochimica et Biophysica Acta Section Body Doc Link PMC2212780 Disease Relevance 0.27 Pain Relevance 0.17
phosphorus and increased ion product [Ca2+×PO4?
Phosphorylation (phosphorus) of Ca2
19) Confidence 0.06 Published 2007 Journal Clinical and Developmental Immunology Section Body Doc Link PMC2248226 Disease Relevance 1.73 Pain Relevance 0

General Comments

This test has worked.

Personal tools
Namespaces

Variants
Actions
Navigation
Toolbox