INT132837

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Context Info
Confidence 0.45
First Reported 2006
Last Reported 2010
Negated 0
Speculated 0
Reported most in Body
Documents 5
Total Number 5
Disease Relevance 1.75
Pain Relevance 1.79

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

Golgi apparatus (Csk) plasma membrane (Csk) kinase activity (Csk)
cytoplasm (Csk)
Anatomy Link Frequency
nucleus accumbens 1
Csk (Mus musculus)
Pain Link Frequency Relevance Heat
Nucleus accumbens 3 99.68 Very High Very High Very High
Morphine 7 98.16 Very High Very High Very High
Inflammatory mediators 5 97.74 Very High Very High Very High
Inflammation 41 91.80 High High
Hyperalgesia 5 88.88 High High
Thermal hyperalgesia 2 86.12 High High
Intracerebroventricular 1 85.68 High High
qutenza 79 75.12 Quite High
Central nervous system 4 74.88 Quite High
calcitonin gene related peptide 14 71.92 Quite High
Disease Link Frequency Relevance Heat
INFLAMMATION 48 97.54 Very High Very High Very High
Breast Cancer 1 97.08 Very High Very High Very High
Adhesions 3 95.28 Very High Very High Very High
Cancer 47 89.84 High High
Hyperalgesia 7 88.88 High High
Nociception 16 82.76 Quite High
Central Nervous System Disease 2 75.20 Quite High
Brain Tumor 6 69.00 Quite High
Dementia 1 68.28 Quite High
Motor Neuron Diseases 1 67.00 Quite High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
We found for the first time that Src family kinase is activated in the nucleus accumbens of mice showing the morphine-induced rewarding effect as compared with that found in saline-treated control mice.
Positive_regulation (activated) of Src family kinase in nucleus accumbens associated with nucleus accumbens and morphine
1) Confidence 0.45 Published 2006 Journal Neuroreport Section Abstract Doc Link 16407755 Disease Relevance 0 Pain Relevance 0.70
With the exception of SEMA5A, FVBP1, IGFBP3, and SELE, these results indicate that chronic treatment with BCG and to a lesser extent acute BCG induced up-regulation of the following genes as was predicted by the mRNA-level analysis: ARL6, CSK, DNAJC5, FAF1, GBP2, GZMA, HLA-DRB1, IL17b, INDO, MAP3K8, SMAD6, TFEB, VCAM1, and WISP2.


Positive_regulation (induced) of CSK
2) Confidence 0.09 Published 2008 Journal BMC Immunol Section Body Doc Link PMC2262873 Disease Relevance 0.11 Pain Relevance 0
Importantly, capsiate suppressed VEGF-induced activation of Src kinase and phosphorylation of its downstream substrates, such as p125(FAK) and VE-cadherin, without affecting autophosphorylation of the VEGF receptor KDR/Flk-1.
Positive_regulation (activation) of Src kinase
3) Confidence 0.07 Published 2008 Journal Cancer Res. Section Abstract Doc Link 18172315 Disease Relevance 0 Pain Relevance 0.14
The inflammatory mediators activate their respective G-protein coupled receptors to initiate secondary messenger pathways resulting in the activation of either PKA [20, 44, 70, 121, 131, 141], PKC [19, 32, 39, 130, 138, 172, 183], MAPK [76, 204], extracellular Ca2+/CaM-dependent kinase II (CaMKII) [83, 149] or Src kinase [77], which phosphorylate TRPV1.
Positive_regulation (activation) of Src kinase associated with inflammatory mediators
4) Confidence 0.02 Published 2008 Journal Current Neuropharmacology Section Body Doc Link PMC2647151 Disease Relevance 0.85 Pain Relevance 0.79
It appears that activation of JAK3, EGFR, Src kinase, and MAP kinase signaling cascades may underlie these effects (Eum et al. 2004, 2006).
Positive_regulation (activation) of Src kinase
5) Confidence 0.01 Published 2010 Journal Environ Health Perspect Section Body Doc Link PMC2854723 Disease Relevance 0.79 Pain Relevance 0.15

General Comments

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