INT120966

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Context Info
Confidence 0.68
First Reported 2004
Last Reported 2010
Negated 0
Speculated 4
Reported most in Abstract
Documents 34
Total Number 38
Disease Relevance 15.15
Pain Relevance 16.59

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

cytosol (Pik3cb) signal transduction (Pik3cb) cell adhesion (Pik3cb)
nucleus (Pik3cb) cytoplasm (Pik3cb)
Anatomy Link Frequency
neurons 2
plasma 1
visceral 1
spinal cord 1
nerve 1
Pik3cb (Rattus norvegicus)
Pain Link Frequency Relevance Heat
opioid receptor 778 100.00 Very High Very High Very High
neuralgia 12 100.00 Very High Very High Very High
Arthritis 52 99.98 Very High Very High Very High
Neuropathic pain 23 99.84 Very High Very High Very High
IPN 8 99.84 Very High Very High Very High
qutenza 35 99.82 Very High Very High Very High
Hyperalgesia 29 99.76 Very High Very High Very High
c fibre 5 99.52 Very High Very High Very High
Inflammation 202 99.36 Very High Very High Very High
Nerve growth factor 14 99.08 Very High Very High Very High
Disease Link Frequency Relevance Heat
Arthritis 54 99.98 Very High Very High Very High
Neuropathic Pain 26 99.84 Very High Very High Very High
Inflammatory Pain 8 99.84 Very High Very High Very High
Hyperalgesia 30 99.76 Very High Very High Very High
INFLAMMATION 229 99.36 Very High Very High Very High
Sepsis 194 99.34 Very High Very High Very High
Death 34 98.22 Very High Very High Very High
Insulin Resistance 79 97.52 Very High Very High Very High
Endotoxemia 6 97.40 Very High Very High Very High
Heart Rate Under Development 2 97.20 Very High Very High Very High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
Similarly, intradermal capsaicin in rats activated PI3K and ERK in C-fiber DRG neurons and epidermal nerve fibers.
Positive_regulation (activated) of PI3K in nerve associated with c fibre and qutenza
1) Confidence 0.68 Published 2004 Journal J. Neurosci. Section Abstract Doc Link 15385613 Disease Relevance 0.73 Pain Relevance 1.28
We examined the activation of PI3K in primary sensory DRG neurons by these inflammatory agents and the contribution of PI3K activation to inflammatory pain.
Spec (examined) Positive_regulation (activation) of PI3K in neurons associated with inflammation and ipn
2) Confidence 0.68 Published 2004 Journal J. Neurosci. Section Abstract Doc Link 15385613 Disease Relevance 0.61 Pain Relevance 0.90
We examined the activation of PI3K in primary sensory DRG neurons by these inflammatory agents and the contribution of PI3K activation to inflammatory pain.
Spec (examined) Positive_regulation (activation) of PI3K in neurons associated with inflammation and ipn
3) Confidence 0.68 Published 2004 Journal J. Neurosci. Section Abstract Doc Link 15385613 Disease Relevance 0.62 Pain Relevance 0.88
Capsaicin and NGF induce phosphorylation of the PI3K downstream target AKT (protein kinase B), which is blocked by the PI3K inhibitors LY294002 and wortmannin, indicative of the activation of PI3K by both agents.
Positive_regulation (activation) of PI3K associated with qutenza
4) Confidence 0.68 Published 2004 Journal J. Neurosci. Section Abstract Doc Link 15385613 Disease Relevance 0.68 Pain Relevance 1.20
Activation of phosphatidylinositol 3-kinase and protein kinase B/Akt in dorsal root ganglia and spinal cord contributes to the neuropathic pain induced by spinal nerve ligation in rats.
Positive_regulation (Activation) of phosphatidylinositol 3-kinase in dorsal root ganglia associated with neuralgia, spinal nerve ligature, neuropathic pain and spinal cord
5) Confidence 0.64 Published 2007 Journal Exp. Neurol. Section Title Doc Link 17628541 Disease Relevance 0.41 Pain Relevance 1.03
STAT3 phosphorylation was also dependent on phosphatidylinositol 3-kinase (PI3K) activation in both tissue and H9C2 cells.
Positive_regulation (activation) of PI3K
6) Confidence 0.56 Published 2006 Journal Am. J. Physiol. Heart Circ. Physiol. Section Abstract Doc Link 16517948 Disease Relevance 0.14 Pain Relevance 0.54
STAT3 phosphorylation was also dependent on phosphatidylinositol 3-kinase (PI3K) activation in both tissue and H9C2 cells.
Positive_regulation (activation) of phosphatidylinositol 3-kinase
7) Confidence 0.56 Published 2006 Journal Am. J. Physiol. Heart Circ. Physiol. Section Abstract Doc Link 16517948 Disease Relevance 0.14 Pain Relevance 0.55
These data suggest that FIT has a prolonged cardioprotective window greater than that of any previously described cardioprotective agent that requires PI3K primarily in the trigger phase but also partially, as a mediator or end effector.
Positive_regulation (requires) of PI3K
8) Confidence 0.49 Published 2005 Journal Am. J. Physiol. Heart Circ. Physiol. Section Abstract Doc Link 15653765 Disease Relevance 0.14 Pain Relevance 0.20
However, the role of PI3K and PI3K-PKB/Akt signal pathway activation in neuropathic pain is still unclear.
Positive_regulation (activation) of PI3K associated with neuropathic pain
9) Confidence 0.47 Published 2007 Journal Exp. Neurol. Section Abstract Doc Link 17628541 Disease Relevance 0.37 Pain Relevance 0.69
Our results indicate that Dex acts on the NTS to elicit hypertension and tachycardia via both a GR-independent interaction with GABA(A) and GABA(B) receptors and a GR-dependent but nontranscriptional mechanism that involves activation of PI3K/Akt pathway.
Positive_regulation (activation) of PI3K associated with heart rate under development, gaba and hypertension
10) Confidence 0.45 Published 2005 Journal Mol. Pharmacol. Section Abstract Doc Link 15523051 Disease Relevance 0.32 Pain Relevance 0.29
Although inhibitors of kinases downstream of PI3K and PLCgamma[glycogen synthetase kinase 3 (GSK3), calmodulin-dependent protein kinase II (CAMII-K) or protein kinase C (PKC)] do not reduce mechanical hyperalgesia, hyperalgesia induced by activation of PI3K was blocked by ERK/MEK inhibitors, suggesting cross-talk from the PI3K to the ERK/MEK signalling pathway.
Positive_regulation (activation) of PI3K associated with hyperalgesia and kinase c
11) Confidence 0.45 Published 2005 Journal Eur. J. Neurosci. Section Abstract Doc Link 16026476 Disease Relevance 0.59 Pain Relevance 1.13
Conceivably, in STZ-treated animals, insulin stimulation of PI3K signaling should restore DA clearance and AMPH-induced DA efflux.
Positive_regulation (stimulation) of PI3K associated with dopamine
12) Confidence 0.42 Published 2007 Journal PLoS Biology Section Body Doc Link PMC2020502 Disease Relevance 0.12 Pain Relevance 0.36
Results indicate 17beta-estradiol may activate the phosphatidylinositol-3-kinase cascade, which subsequently phosphorylates the NR2B subunit, via spinal estrogen receptors ERalpha/ERbeta, to facilitate NMDA-dependent cross-organ sensitization, which is presumed to underlie pelvic viscero-visceral referred pain.
Spec (may) Positive_regulation (activate) of phosphatidylinositol-3-kinase in visceral associated with referred pain
13) Confidence 0.40 Published 2010 Journal J. Neurochem. Section Abstract Doc Link 20067569 Disease Relevance 0.28 Pain Relevance 0.32
Previous studies have demonstrated that skeletal muscle and adipose tissue contribute to IL-6 production during endotoxemia [45], [46], [47], and the anti-inflammatory effects of atorvastatin on IL-6 production in sepsis may be the result of the direct activation of PI3K pathway in these tissues.
Positive_regulation (activation) of PI3K in adipose tissue associated with endotoxemia, inflammation, obesity and sepsis
14) Confidence 0.36 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2997789 Disease Relevance 1.12 Pain Relevance 0.22
These findings are consistent with the observation that activation and internalization of a GPCR can be regulated by activation of the PI3K/AKT pathway [43].
Positive_regulation (activation) of PI3K
15) Confidence 0.34 Published 2010 Journal Mol Pain Section Body Doc Link PMC2908066 Disease Relevance 0 Pain Relevance 0.38
Activation of the PI3K/AKT pathway was tested by exposing SKNMCs to the selective PI3K inhibitor LY294002 (50 ?
Positive_regulation (Activation) of PI3K
16) Confidence 0.34 Published 2010 Journal Mol Pain Section Body Doc Link PMC2908066 Disease Relevance 0 Pain Relevance 0.38
In the present study, we provide evidence that TCA, through activation of GPCR(s) and the PI3K/PDK-1/AKT pathway (insulin signaling pathway), can regulate gluconeogenic genes.
Positive_regulation (activation) of PI3K
17) Confidence 0.26 Published 2010 Journal Journal of Lipid Research Section Body Doc Link PMC2903791 Disease Relevance 0.20 Pain Relevance 0.25
Moreover, it appears that activation of the PI3K/PDK-1/PKC?
Spec (appears) Positive_regulation (activation) of PI3K
18) Confidence 0.26 Published 2010 Journal Journal of Lipid Research Section Body Doc Link PMC2903791 Disease Relevance 0.20 Pain Relevance 0.21
IPC activates PI3-kinase which facilitates phosphorylation and activation of the protein kinase Akt through its mediator PDK-1 [1].
Positive_regulation (activates) of PI3-kinase
19) Confidence 0.26 Published 2010 Journal Basic Res Cardiol Section Body Doc Link PMC3012213 Disease Relevance 0.20 Pain Relevance 0.06
Especially, Weiner and Chun demonstrated that LPA1 was expressed by postnatal SCs, and that LPA promotes SC survival via LPA1 activation and a pathway including Gi, PI3K (phosphoinositide-3-kinase) and Akt [23].
Positive_regulation (activation) of PI3K in SCs
20) Confidence 0.24 Published 2006 Journal Acta Histochemica et Cytochemica Section Body Doc Link PMC1828080 Disease Relevance 0.16 Pain Relevance 0.09

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