INT111946

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Context Info
Confidence 0.66
First Reported 2003
Last Reported 2009
Negated 0
Speculated 0
Reported most in Body
Documents 8
Total Number 22
Disease Relevance 11.50
Pain Relevance 1.53

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

extracellular matrix organization (PTK2) embryo development (PTK2) microtubule organizing center (PTK2)
cytoplasm (PTK2) signal transducer activity (PTK2) cytosol (PTK2)
Anatomy Link Frequency
myometrium 4
AsPC-1 4
colon 3
MCF7 2
liver 1
PTK2 (Homo sapiens)
Pain Link Frequency Relevance Heat
Kinase C 1 100.00 Very High Very High Very High
Opioid 11 99.98 Very High Very High Very High
Kappa opioid receptor 8 99.74 Very High Very High Very High
antagonist 30 91.52 High High
agonist 5 80.64 Quite High
Neurotransmitter 1 69.28 Quite High
MU agonist 1 68.84 Quite High
opioid receptor 2 67.00 Quite High
opiate 1 60.24 Quite High
palliative 15 59.72 Quite High
Disease Link Frequency Relevance Heat
Adhesions 253 100.00 Very High Very High Very High
Cancer 322 99.92 Very High Very High Very High
Pancreatic Cancer 720 99.84 Very High Very High Very High
Bordatella Infection 1 98.52 Very High Very High Very High
Malignant Neoplastic Disease 45 97.76 Very High Very High Very High
Metastasis 73 97.24 Very High Very High Very High
Apoptosis 574 96.12 Very High Very High Very High
Skin Cancer 15 94.88 High High
Breast Cancer 23 93.04 High High
Lung Cancer 15 81.76 Quite High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
These results indicate that induced FAK phosphorylation is involved in LN-mediated chemoresistance to Gem and further confirm FAK as a promising therapeutic target in pancreatic cancer.
Positive_regulation (induced) of Phosphorylation (phosphorylation) of FAK associated with pancreatic cancer
1) Confidence 0.66 Published 2009 Journal Mol Cancer Section Body Doc Link PMC2806309 Disease Relevance 0.49 Pain Relevance 0
Pretreatment of MCF7 cells with the specific PI-3 kinase inhibitor wortmannin abolished both the activation of Rac1 and actin reorganization, while the opioid-induced phosphorylation of FAK and vinculin remained unaffected.
Positive_regulation (induced) of Phosphorylation (phosphorylation) of FAK in MCF7 associated with malignant neoplastic disease and opioid
2) Confidence 0.64 Published 2003 Journal Exp. Cell Res. Section Abstract Doc Link 12878162 Disease Relevance 0.66 Pain Relevance 0.79
Similarly, in Aspc-1 cells, LN-induced FAK phosphorylation was accompanied by Akt but not ERK activation, and specific inhibition of FAK phosphorylation decreased LN-induced Akt activation.
Positive_regulation (induced) of Phosphorylation (phosphorylation) of FAK
3) Confidence 0.48 Published 2009 Journal Mol Cancer Section Body Doc Link PMC2806309 Disease Relevance 0.36 Pain Relevance 0
These results demonstrate that constitutive FAK phosphorylation contributes to the intrinsic chemoresistance to Gem in pancreatic cancer cells.
Positive_regulation (contributes) of Phosphorylation (phosphorylation) of FAK associated with pancreatic cancer
4) Confidence 0.48 Published 2009 Journal Mol Cancer Section Body Doc Link PMC2806309 Disease Relevance 0.65 Pain Relevance 0
In our study, corresponding with the alteration of Akt, pBad (pS136) was regulated by constitutive and induced FAK phosphorylation in pancreatic cancer cells.
Positive_regulation (induced) of Phosphorylation (phosphorylation) of FAK associated with pancreatic cancer
5) Confidence 0.48 Published 2009 Journal Mol Cancer Section Body Doc Link PMC2806309 Disease Relevance 0.89 Pain Relevance 0
M PF-228 was sufficient to efficiently block both constitutive FAK phosphorylation in Panc-1 cells and LN-induced FAK phosphorylation in Aspc-1 cells.
Positive_regulation (induced) of Phosphorylation (phosphorylation) of FAK
6) Confidence 0.48 Published 2009 Journal Mol Cancer Section Body Doc Link PMC2806309 Disease Relevance 0.42 Pain Relevance 0
PF-228 could inhibit both constitutive and LN-induced FAK phosphorylation in a dose-dependent manner (Fig. 11A-B). 1 ?
Positive_regulation (induced) of Phosphorylation (phosphorylation) of FAK
7) Confidence 0.48 Published 2009 Journal Mol Cancer Section Body Doc Link PMC2806309 Disease Relevance 0.40 Pain Relevance 0
We used PF-228 to downregulate constitutive FAK phosphorylation in Panc-1 cells and LN-induced FAK phosphorylation in Aspc-1 cells respectively.
Positive_regulation (induced) of Phosphorylation (phosphorylation) of FAK
8) Confidence 0.48 Published 2009 Journal Mol Cancer Section Body Doc Link PMC2806309 Disease Relevance 0.37 Pain Relevance 0
These data indicate that Akt might be involved in the intrinsic chemoresistance mediated by FAK phosphorylation.
Positive_regulation (mediated) of Phosphorylation (phosphorylation) of FAK
9) Confidence 0.48 Published 2009 Journal Mol Cancer Section Body Doc Link PMC2806309 Disease Relevance 0.57 Pain Relevance 0
The role of LN-induced FAK phosphorylation in LN-mediated Gem chemoresistance was further confirmed by using the more specific inhibitor of FAK phosphorylation, PF-228.
Positive_regulation (induced) of Phosphorylation (phosphorylation) of FAK
10) Confidence 0.48 Published 2009 Journal Mol Cancer Section Body Doc Link PMC2806309 Disease Relevance 0.63 Pain Relevance 0
A low level of constitutively activated FAK and Akt was found in AsPC-1 cells, and a rapid and strong stimulation of FAK and Akt phosphorylation was induced by LN.
Positive_regulation (stimulation) of Phosphorylation (phosphorylation) of FAK in AsPC-1
11) Confidence 0.48 Published 2009 Journal Mol Cancer Section Body Doc Link PMC2806309 Disease Relevance 0.23 Pain Relevance 0
These results indicated that in AsPC-1 cells, LN-induced FAK phosphorylation mediated the intrinsic chemoresistance to Gem, and this effect might be related with the regulation of survivin and pBad (pS136) level

Effects of PF-228 on Gem-induced apoptosis in pancreatic cancer cells

Positive_regulation (induced) of Phosphorylation (phosphorylation) of FAK in AsPC-1 associated with pancreatic cancer and apoptosis
12) Confidence 0.48 Published 2009 Journal Mol Cancer Section Body Doc Link PMC2806309 Disease Relevance 0.52 Pain Relevance 0
FAK expression or phosphorylation is elevated in ovarian, breast, head and neck, thyroid, esophageal, colon, liver and pancreatic cancers, indicating that FAK might be a novel therapeutic target and prognostic marker for these malignancies [12,13,17,23].
Positive_regulation (elevated) of Phosphorylation (phosphorylation) of FAK in colon associated with pancreatic cancer
13) Confidence 0.44 Published 2009 Journal Mol Cancer Section Body Doc Link PMC2806309 Disease Relevance 0.69 Pain Relevance 0
Comparable protein levels of total FAK were found in these cell lines, whereas different levels of constitutive FAK phosphorylation were detected in these cell lines.
Positive_regulation (detected) of Phosphorylation (phosphorylation) of FAK
14) Confidence 0.44 Published 2009 Journal Mol Cancer Section Body Doc Link PMC2806309 Disease Relevance 0.39 Pain Relevance 0
FAK expression and (or) phosphorylation was elevated in a variety of cancers and frequently correlated with malignant or metastatic disease and poor patient prognosis [12,13].
Positive_regulation (elevated) of Phosphorylation (phosphorylation) of FAK associated with malignant neoplastic disease, cancer and metastasis
15) Confidence 0.44 Published 2009 Journal Mol Cancer Section Body Doc Link PMC2806309 Disease Relevance 1.52 Pain Relevance 0.06
Consistently, activated kappa-opioid receptor induced Src stimulation and FAK autophosphorylation and promoted the formation of Src-FAK complex.
Positive_regulation (stimulation) of Phosphorylation (autophosphorylation) of FAK associated with kappa opioid receptor
16) Confidence 0.44 Published 2004 Journal J. Pharmacol. Exp. Ther. Section Abstract Doc Link 14996948 Disease Relevance 0.17 Pain Relevance 0.46
This effect was regulated by early phosphorylation of FAK and subsequent PI-3K and Rac1 activation.
Positive_regulation (activation) of Phosphorylation (phosphorylation) of FAK
17) Confidence 0.39 Published 2007 Journal Cell. Physiol. Biochem. Section Abstract Doc Link 17982280 Disease Relevance 0.32 Pain Relevance 0.14
Elevations of tyrosine phosphorylation of FAK and Cas appeared to be transient in the myometrial stretch experiments.
Positive_regulation (Elevations) of Phosphorylation (phosphorylation) of FAK
18) Confidence 0.26 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2759504 Disease Relevance 0.22 Pain Relevance 0
Here we have shown that the molecular mechanisms of stretch-induced activation of human myometrium include (1) increased tyrosine phosphorylation of FAK, and Cas, hallmarks of focal adhesion signaling, (2) increased association of, or tyrosine phosphorylation of, ?
Positive_regulation (increased) of Phosphorylation (phosphorylation) of FAK in myometrium associated with adhesions
19) Confidence 0.26 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2759504 Disease Relevance 0.36 Pain Relevance 0
Here we have shown that the molecular mechanisms of stretch-induced activation of human myometrium include (1) increased tyrosine phosphorylation of FAK, and Cas, hallmarks of focal adhesion signaling, (2) increased association of, or tyrosine phosphorylation of, ?
Positive_regulation (increased) of Phosphorylation (phosphorylation) of FAK in myometrium associated with adhesions
20) Confidence 0.18 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2759504 Disease Relevance 0.36 Pain Relevance 0

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