INT55259

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Context Info
Confidence 0.49
First Reported 1994
Last Reported 2010
Negated 0
Speculated 1
Reported most in Body
Documents 9
Total Number 11
Disease Relevance 1.87
Pain Relevance 3.40

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

cytosol (Calm2) nucleoplasm (Calm2) cytoskeleton (Calm2)
cell cycle (Calm2) cellular_component (Calm2) biological_process (Calm2)
Anatomy Link Frequency
neurons 3
spinal 1
testis 1
olfactory bulb 1
Calm2 (Rattus norvegicus)
Pain Link Frequency Relevance Heat
Kinase C 80 100.00 Very High Very High Very High
sodium channel 6 99.76 Very High Very High Very High
Opioid 5 99.68 Very High Very High Very High
Dopamine 4 99.64 Very High Very High Very High
Nicotine 7 98.52 Very High Very High Very High
Spinal cord 1 96.40 Very High Very High Very High
Enkephalin 2 96.20 Very High Very High Very High
agonist 25 94.52 High High
opiate 1 94.20 High High
conotoxin 1 94.08 High High
Disease Link Frequency Relevance Heat
Death 4 99.40 Very High Very High Very High
Bordatella Infection 3 99.14 Very High Very High Very High
Toxicity 2 97.16 Very High Very High Very High
Status Epilepticus 114 92.88 High High
Epilepsy 32 92.80 High High
Urological Neuroanatomy 1 88.00 High High
Nociception 1 84.40 Quite High
Convulsion 36 76.00 Quite High
Gliosis 8 56.80 Quite High
INFLAMMATION 25 55.84 Quite High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
The result indicated that 10 nmol/L-1 mumol/L NDAP produced dose-dependent decrease in CaM activity of rat spinal synaptosomes (P < 0.01).
Negative_regulation (decrease) of CaM in spinal
1) Confidence 0.49 Published 1994 Journal Sheng Li Xue Bao Section Abstract Doc Link 7973792 Disease Relevance 0 Pain Relevance 0.40
CaM can bind to the C-termini of voltage-gated sodium channels and modulate their functional properties; therefore we investigated if TFP modulation of sodium channels was due to CaM inhibition.
Negative_regulation (inhibition) of CaM associated with sodium channel
2) Confidence 0.44 Published 2006 Journal J. Neurophysiol. Section Abstract Doc Link 16807347 Disease Relevance 0.08 Pain Relevance 0.58
CONCLUSION: Morphine dependence can induce testis cell apoptosis, an increase in testis NOS positive cells, a decrease in CaM content and the activity of SOD and GSHPx in the testis.
Negative_regulation (decrease) of CaM in testis
3) Confidence 0.29 Published 2004 Journal Zhonghua Nan Ke Xue Section Body Doc Link 15595686 Disease Relevance 0 Pain Relevance 0
In vivo treatment of olfactory bulb with pertussis toxin prevents both opioid and muscarinic inhibition of Ca2+/CaM- and FSK-stimulated enzyme activities.
Negative_regulation (inhibition) of CaM in olfactory bulb associated with bordatella infection and opioid
4) Confidence 0.28 Published 1994 Journal J. Neurochem. Section Abstract Doc Link 8207425 Disease Relevance 0.16 Pain Relevance 0.72
With Siah1a and Siah1a + CaM inhibition was 7 ± 6% (n = 3) and 30 ± 18% (n = 3), respectively.
Negative_regulation (inhibition) of CaM
5) Confidence 0.24 Published 2001 Journal BMC Neurosci Section Body Doc Link PMC58838 Disease Relevance 0 Pain Relevance 0
CaM binding to both group I and group III mGluRs can be inhibited by serine/threonine phosphorylation at specific sites [25,28].
Negative_regulation (inhibited) of CaM
6) Confidence 0.24 Published 2001 Journal BMC Neurosci Section Body Doc Link PMC58838 Disease Relevance 0 Pain Relevance 0
Inhibitors of phospholipase A(2) (PLA(2)), COX and phospholipase C (PLC), calcium/calmodulin (CaM), NOS and soluble guanylate cyclase prevent the carbachol effect.
Negative_regulation (Inhibitors) of CaM
7) Confidence 0.21 Published 2005 Journal Neuropharmacology Section Abstract Doc Link 15814109 Disease Relevance 0.09 Pain Relevance 0.07
The reduced CaM expression in our study is also interesting since there is extensive evidence that CaM plays a critical role in the induction of cell death following Ca2+ overload, and inhibition of CaM function can protect neurons from death [48], [49].
Negative_regulation (inhibition) of CaM in neurons associated with death
8) Confidence 0.20 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2873964 Disease Relevance 0.91 Pain Relevance 0.10
Furthermore, PEP-19 has shown neuroprotective properties in cell cultures, these possibly being mediated through CaM inhibition that could lead to enhanced resistance of neurons to calcium-mediated toxicity [46], [47], which makes it tempting to speculate that this protein is neuroprotective also in our SE model.
Negative_regulation (inhibition) of CaM in neurons associated with toxicity and status epilepticus
9) Confidence 0.20 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2873964 Disease Relevance 0.63 Pain Relevance 0.12
Finally, inhibition of protein kinase C also abolished the nicotine-mediated enhancement of amphetamine-stimulated dopamine release, whereas inhibitors of Ca(2+)/calmodulin kinase II did not.
Negative_regulation (inhibitors) of calmodulin kinase II associated with dopamine, kinase c and nicotine
10) Confidence 0.05 Published 2001 Journal J. Neurochem. Section Abstract Doc Link 11331413 Disease Relevance 0 Pain Relevance 0.96
Increased synaptic activity induced by picrotoxin in the hippocampal neurons also resulted in the translocation of MARCKS and inhibitor studies implicate both a PKC and CaM regulatory component under these conditions.
Spec (implicate) Negative_regulation (implicate) of CaM in neurons associated with kinase c
11) Confidence 0.03 Published 2007 Journal Journal of Neurochemistry Section Body Doc Link PMC2658029 Disease Relevance 0 Pain Relevance 0.46

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