INT89639

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Context Info
Confidence 0.48
First Reported 2000
Last Reported 2006
Negated 0
Speculated 0
Reported most in Abstract
Documents 5
Total Number 6
Disease Relevance 0.66
Pain Relevance 1.78

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

cell differentiation (CAMK2G) cytosol (CAMK2G) nucleoplasm (CAMK2G)
plasma membrane (CAMK2G)
Anatomy Link Frequency
oocytes 2
CAMK2G (Homo sapiens)
Pain Link Frequency Relevance Heat
Kinase C 164 100.00 Very High Very High Very High
opioid receptor 16 96.76 Very High Very High Very High
Enkephalin 4 93.80 High High
agonist 12 91.32 High High
tetrodotoxin 2 79.28 Quite High
long-term potentiation 16 77.92 Quite High
nMDA receptor 6 76.52 Quite High
Central nervous system 14 42.68 Quite Low
Neurobehavioral 12 39.68 Quite Low
Neurotransmitter 12 21.92 Low Low
Disease Link Frequency Relevance Heat
Virus Diseases 188 92.48 High High
Infection 40 84.12 Quite High
Borna Disease 10 50.00 Quite Low
Sprains And Strains 6 48.40 Quite Low
Cognitive Disorder 6 40.24 Quite Low
Disease 10 31.08 Quite Low
Neurodegenerative Disease 4 29.96 Quite Low
Targeted Disruption 4 23.04 Low Low
INFLAMMATION 6 5.00 Very Low Very Low Very Low
Acquired Immune Deficiency Syndrome Or Hiv Infection 4 5.00 Very Low Very Low Very Low

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
In the present study, we show that the injection of active CaMK II in Xenopus laevis oocytes led to the desensitization of S261A but not S266A receptor mutant, indicating that S266 is the primary CaMK II phosphorylation site of the rMOR1.
Phosphorylation (phosphorylation) of CaMK II in oocytes
1) Confidence 0.48 Published 2000 Journal Mol. Pharmacol. Section Abstract Doc Link 10908300 Disease Relevance 0 Pain Relevance 0.29
In the present study, we show that the injection of active CaMK II in Xenopus laevis oocytes led to the desensitization of S261A but not S266A receptor mutant, indicating that S266 is the primary CaMK II phosphorylation site of the rMOR1.
Phosphorylation (phosphorylation) of CaMK II in oocytes
2) Confidence 0.48 Published 2000 Journal Mol. Pharmacol. Section Abstract Doc Link 10908300 Disease Relevance 0 Pain Relevance 0.28
We have recently shown that the substitution of two putative Ca(2+)/calmodulin-dependent protein kinase II (CaMK II) phosphorylation sites, S261 and S266, by alanines in the third intracellular loop of the rat mu-opioid receptor (rMOR1) confers resistance to CaMK II-induced receptor desensitization.
Phosphorylation (phosphorylation) of CaMK II associated with opioid receptor
3) Confidence 0.37 Published 2000 Journal Mol. Pharmacol. Section Abstract Doc Link 10908300 Disease Relevance 0 Pain Relevance 0.30
We have recently shown that the substitution of two putative Ca(2+)/calmodulin-dependent protein kinase II (CaMK II) phosphorylation sites, S261 and S266, by alanines in the third intracellular loop of the rat mu-opioid receptor (rMOR1) confers resistance to CaMK II-induced receptor desensitization.
Phosphorylation (phosphorylation) of calmodulin-dependent protein kinase II associated with opioid receptor
4) Confidence 0.32 Published 2000 Journal Mol. Pharmacol. Section Abstract Doc Link 10908300 Disease Relevance 0 Pain Relevance 0.30
In particular, extracellular-regulated kinase (ERK) 1/2, protein kinase A (PKA), Ca2+/calmodulin-dependent kinase (CaMK) II, and PKC phosphorylate presynaptic proteins that modulate SV recycling [28,29].
Phosphorylation (phosphorylate) of CaMK associated with kinase c
5) Confidence 0.06 Published 2006 Journal PLoS Pathogens Section Body Doc Link PMC1401496 Disease Relevance 0.61 Pain Relevance 0.20
Antibodies specific for synapsin I phosphorylated by CaMK II at site 3 (clone RU19), or by PKA and CaMK I at site 1 (clone G257) were provided by P.
Phosphorylation (phosphorylated) of CaMK
6) Confidence 0.03 Published 2006 Journal PLoS Pathogens Section Body Doc Link PMC1401496 Disease Relevance 0.05 Pain Relevance 0.40

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