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Context Info
Confidence 0.15
First Reported 2004
Last Reported 2010
Negated 1
Speculated 0
Reported most in Body
Documents 5
Total Number 6
Disease Relevance 1.30
Pain Relevance 0.03

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

cytosol (PIK3CG) plasma membrane (PIK3CG) cytoplasm (PIK3CG)
PIK3CG (Homo sapiens)
Pain Link Frequency Relevance Heat
antagonist 3 66.40 Quite High
anesthesia 1 42.92 Quite Low
addiction 10 5.00 Very Low Very Low Very Low
fibrosis 7 5.00 Very Low Very Low Very Low
Pain 5 5.00 Very Low Very Low Very Low
cytokine 4 5.00 Very Low Very Low Very Low
Antihistamine 4 5.00 Very Low Very Low Very Low
Inflammation 3 5.00 Very Low Very Low Very Low
nud 2 5.00 Very Low Very Low Very Low
palliative 2 5.00 Very Low Very Low Very Low
Disease Link Frequency Relevance Heat
Endometrial Cancer 20 87.88 High High
Adenocarcinoma 3 85.52 High High
Apoptosis 24 80.16 Quite High
Cancer 80 79.96 Quite High
Stomach Cancer 9 76.40 Quite High
Lung Cancer 2 73.64 Quite High
Telangiectasia 17 72.08 Quite High
Prostate Cancer 55 71.64 Quite High
Breast Cancer 61 64.96 Quite High
Malignant Neoplastic Disease 5 63.92 Quite High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
PI 3-K inhibition in RL 95-2 and Ishikawa cells directly blocked Akt phosphorylation and caused a reduction of COX-2 mRNA and protein [42].
PI 3-K Neg (inhibition) Binding (inhibition) of
1) Confidence 0.15 Published 2004 Journal Mol Cancer Section Body Doc Link PMC394342 Disease Relevance 0.47 Pain Relevance 0
One key difference between the modeling and the Balk et al. study was the binding of activated AR with the regulatory subunit of PI3K.
PI3K Binding (binding) of
2) Confidence 0.07 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2812491 Disease Relevance 0.15 Pain Relevance 0
In addition to direct AR binding, PI3K (and subsequently TOR) can be activated through receptor adaptor complexes such as those associated with Her2.
PI3K Binding (binding) of
3) Confidence 0.06 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2812491 Disease Relevance 0.13 Pain Relevance 0
Recent study clearly confirmed that almost one dozen of factors such as SHP-1, Grd2, Grb2, phosphatidylinositol 3-OH kinase (PI3K), have also binding abilities to CagA phosphorylation sites [34].
PI3K Binding (binding) of
4) Confidence 0.05 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2768901 Disease Relevance 0.22 Pain Relevance 0
The protein contains several important domains such as 1) the C-terminal protein kinase domain (PI3K-domain), 2) the substrate binding domain in the N-terminal of the protein necessary for activation of p53 in response to DNA damage, 3)the FAT domain – common for the PI3K-like family members FRAP, ATM and TRAPP, 4) a proline rich region shown to bind c-Abl and 5) an incomplete leucine zipper.
PI3K Binding (bind) of
5) Confidence 0.05 Published 2007 Journal Radiat Oncol Section Body Doc Link PMC1971057 Disease Relevance 0.34 Pain Relevance 0
As a result, adapter proteins such as Grb2, Ras-specific GTPase-activating protein (GAP), and phosphatidylinositol-3-kinase (PI-3K), can interact with the phosphotyrosine residues and stimulate downstream signaling, including the Ras-MAPK and PI-3K-Akt pathways.
PI-3K Binding (interact) of
6) Confidence 0.03 Published 2007 Journal Biologics : Targets & Therapy Section Body Doc Link PMC2721306 Disease Relevance 0 Pain Relevance 0.03

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