INT120401

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Context Info
Confidence 0.45
First Reported 2004
Last Reported 2010
Negated 0
Speculated 1
Reported most in Body
Documents 33
Total Number 34
Disease Relevance 14.89
Pain Relevance 7.37

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 (PIK3CD) signal transduction (PIK3CD) plasma membrane (PIK3CD)
Anatomy Link Frequency
T cell 2
lymphocyte 1
bladder 1
spleen 1
HT-1080 1
PIK3CD (Homo sapiens)
Pain Link Frequency Relevance Heat
Kinase C 69 100.00 Very High Very High Very High
cytokine 192 99.98 Very High Very High Very High
bradykinin 156 98.84 Very High Very High Very High
COX2 6 98.76 Very High Very High Very High
Opioid 403 98.70 Very High Very High Very High
Inflammation 601 97.28 Very High Very High Very High
IPN 116 97.20 Very High Very High Very High
Inflammatory response 28 96.12 Very High Very High Very High
Calcium channel 14 94.12 High High
Pain 179 92.72 High High
Disease Link Frequency Relevance Heat
Hyperglycemia 76 99.98 Very High Very High Very High
Adhesions 64 99.74 Very High Very High Very High
Cancer 813 99.56 Very High Very High Very High
Necrosis 59 99.28 Very High Very High Very High
Lung Cancer 81 98.68 Very High Very High Very High
Bladder Cancer 4 98.52 Very High Very High Very High
Targeted Disruption 28 98.12 Very High Very High Very High
Solid Tumor 18 97.72 Very High Very High Very High
INFLAMMATION 643 97.28 Very High Very High Very High
Inflammatory Pain 116 97.20 Very High Very High Very High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
Aberrations leading to increased activation of the PI3K/AKT pathway are common in human cancers and are reviewed in [31].
Positive_regulation (activation) of PI3K associated with cancer
1) Confidence 0.45 Published 2010 Journal Genome Biol Section Body Doc Link PMC2945784 Disease Relevance 0.73 Pain Relevance 0
The results suggest that EGFR, PI3K, and ERK are required for the proliferative effects of BK.
Positive_regulation (required) of PI3K associated with bradykinin
2) Confidence 0.43 Published 2004 Journal J. Cell. Physiol. Section Abstract Doc Link 15281091 Disease Relevance 0 Pain Relevance 0.33
Arbiser et al. reported that Solenopsin, the alkaloidal component of the fire ant, prevented angiogenesis by inhibiting the activation of PI3K and the phosphorylation of AKT [29].
Positive_regulation (activation) of PI3K
3) Confidence 0.35 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2925949 Disease Relevance 0.30 Pain Relevance 0.03
Thus, we examined the potential role of PO on activation of PI3K and AKT in HT-1080 cells.
Spec (examined) Positive_regulation (activation) of PI3K in HT-1080
4) Confidence 0.35 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2925949 Disease Relevance 0.39 Pain Relevance 0.03
As LY294002 is strictly specific to PI3K [31], it is highly plausible that PI3K is activated in the LPS-activated pathway.
Positive_regulation (activated) of PI3K
5) Confidence 0.31 Published 2010 Journal J Inflamm (Lond) Section Body Doc Link PMC2819999 Disease Relevance 0.21 Pain Relevance 0
We show that bradykinin promotes resensitization of P2Y purinergic receptors via activation of PI3K and the phosphatase A2 pathways.


Positive_regulation (activation) of PI3K associated with bradykinin
6) Confidence 0.31 Published 2010 Journal Cancer Cell Int Section Body Doc Link PMC2955562 Disease Relevance 0.50 Pain Relevance 0.28
The activation of PI3K/Akt pathway may lead to the phosphorylation of Bad, which is consequently sequestrated in the cytoplasm by 14-3-3 protein and, in this way, inhibited in its pro-apoptotic function [51].
Positive_regulation (activation) of PI3K associated with apoptosis
7) Confidence 0.30 Published 2010 Journal International Journal of Cell Biology Section Body Doc Link PMC2841246 Disease Relevance 0.89 Pain Relevance 0
B2R activation also activates PKC, phosphatase A2, phospholipase C, and phosphoinositide 3-kinase (PI3K), and stimulates production of nitric oxide [19,20].
Positive_regulation (activates) of PI3K associated with kinase c
8) Confidence 0.23 Published 2010 Journal Cancer Cell Int Section Body Doc Link PMC2955562 Disease Relevance 0.54 Pain Relevance 0.32
Interestingly, activation of PI3K can also increase RhoA activation [68].
Positive_regulation (activation) of PI3K
9) Confidence 0.22 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2909203 Disease Relevance 0 Pain Relevance 0
As a result of VEGFR2 activation, PI3K is activated and favors the catalysis of PtdIns(3,4)P2 or PIP2 to PtdIns(3,4,5)P3 or PIP3 (Fig 7).
Positive_regulation (activation) of PI3K
10) Confidence 0.22 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2909203 Disease Relevance 0 Pain Relevance 0
PI3K activation by growth factors including vascular endothelial growth factor (VEGF) is known to be crucial in angiogenesis.
Positive_regulation (activation) of PI3K
11) Confidence 0.22 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2909203 Disease Relevance 0.11 Pain Relevance 0
EP2 and EP4 receptors are coupled with G proteins which activate adenylate cyclase, leading to an increase of intracellular cAMP [41]. cAMP is then able to activate kinases such as protein kinase A (PKA) or PI3K for example, and also GSK3 leading to an activation of ?
Positive_regulation (activate) of PI3K
12) Confidence 0.22 Published 2010 Journal International Journal of Cell Biology Section Body Doc Link PMC2841246 Disease Relevance 0.82 Pain Relevance 0.03
Other studies demonstrated that COX-2 inhibits anoikis via activation of PI3K/Akt pathway, as the case of a human bladder cancer cell line expressing COX-2 [40].
Positive_regulation (activation) of PI3K in bladder associated with bladder cancer
13) Confidence 0.22 Published 2010 Journal International Journal of Cell Biology Section Body Doc Link PMC2841246 Disease Relevance 0.77 Pain Relevance 0
In addition, activation via CD28 is very important for re-expression of the TCR, for the recruitment and stabilization of T cell lipid rafts to the “immunological synapse” and for the stimulation of the phosphoinositide kinase-3 (PI3K) signaling pathway (Tavano et al 2004).
Positive_regulation (stimulation) of PI3K in T cell
14) Confidence 0.20 Published 2007 Journal Clinical Interventions in Aging Section Body Doc Link PMC2684090 Disease Relevance 0.48 Pain Relevance 0
In addition, activation via CD28 is very important for re-expression of the TCR, for the recruitment and stabilization of T cell lipid rafts to the “immunological synapse” and for the stimulation of the phosphoinositide kinase-3 (PI3K) signaling pathway (Tavano et al 2004).
Positive_regulation (stimulation) of phosphoinositide kinase-3 in T cell
15) Confidence 0.20 Published 2007 Journal Clinical Interventions in Aging Section Body Doc Link PMC2684090 Disease Relevance 0.48 Pain Relevance 0
Fak is phosphorylated upon integrin adhesion, leading to activation of other signaling pathways like PI3K, MAPK.
Positive_regulation (activation) of PI3K associated with adhesions
16) Confidence 0.20 Published 2010 Journal International Journal of Cell Biology Section Body Doc Link PMC2841246 Disease Relevance 0.62 Pain Relevance 0
FPR is known to signal through Gi proteins stimulating phospholipase C leading to mobilization of Ca2+ from intracellular stores and to activation of PI3K [24].
Positive_regulation (activation) of PI3K
17) Confidence 0.18 Published 2009 Journal PLoS Pathogens Section Body Doc Link PMC2657213 Disease Relevance 0.07 Pain Relevance 0.96
This requires activation of FPR as well as intracellular Ca2+ mobilization and PI3K activation, while TLR-2 and -4 do not seem to be involved.
Positive_regulation (activation) of PI3K
18) Confidence 0.18 Published 2009 Journal PLoS Pathogens Section Body Doc Link PMC2657213 Disease Relevance 1.37 Pain Relevance 1.10
Normally, stimulation of NO production by insulin is mediated by signaling pathways involving activation of Phosphoinositide-3 (PI-3) kinase leading to phosphorylation of eNOS.
Positive_regulation (activation) of Phosphoinositide-3
19) Confidence 0.17 Published 2010 Journal Mediators of Inflammation Section Body Doc Link PMC2903979 Disease Relevance 1.19 Pain Relevance 0.06
We propose that CCM development may result from the dysregulation of the VEGF/PI3K signaling pathway through PDCD10- PtdIns(3,4,5)P3 interaction.
Positive_regulation (dysregulation) of PI3K
20) Confidence 0.16 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2909203 Disease Relevance 0 Pain Relevance 0

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