INT292497

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Context Info
Confidence 0.05
First Reported 2009
Last Reported 2009
Negated 0
Speculated 0
Reported most in Body
Documents 1
Total Number 13
Disease Relevance 7.24
Pain Relevance 0

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) pigmentation (Mlph)
Anatomy Link Frequency
AsPC-1 16
Mlph (Mus musculus)
PTK2 (Homo sapiens)
Pain Link Frequency Relevance Heat
palliative 13 5.00 Very Low Very Low Very Low
Disease Link Frequency Relevance Heat
Apoptosis 481 99.18 Very High Very High Very High
Pancreatic Cancer 624 97.80 Very High Very High Very High
Adhesions 91 92.72 High High
Cancer 221 79.92 Quite High
Malignant Neoplastic Disease 26 66.96 Quite High
Lung Cancer 13 62.60 Quite High
Death 13 28.92 Quite Low
Breast Cancer 13 8.76 Low Low
Metastasis 52 5.00 Very Low Very Low Very Low
Disease 13 5.00 Very Low Very Low Very Low

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
Our studies found that LN induced FAK phosphorylation in a time-dependent manner in AsPC-1 cells, and FAK phosphorylation inhibition by either RNAi or FRNK overexpression antagonized the effect of LN on Gem chemoresistance.
LN Positive_regulation (induced) of Phosphorylation (phosphorylation) of FAK in AsPC-1
1) Confidence 0.05 Published 2009 Journal Mol Cancer Section Body Doc Link PMC2806309 Disease Relevance 0.85 Pain Relevance 0
These results indicated that in AsPC-1 cells, LN induced FAK and Akt phosphorylation in a time-dependent manner, and LN-induced Akt phosphorylation was mediated by FAK activation.


LN Positive_regulation (induced) of Phosphorylation (phosphorylation) of FAK in AsPC-1
2) Confidence 0.05 Published 2009 Journal Mol Cancer Section Body Doc Link PMC2806309 Disease Relevance 0.22 Pain Relevance 0
LN induces the phosphorylation of FAK and its downstream kinase Akt in AsPC-1 cells
LN Positive_regulation (induces) of Phosphorylation (phosphorylation) of FAK in AsPC-1
3) Confidence 0.04 Published 2009 Journal Mol Cancer Section Body Doc Link PMC2806309 Disease Relevance 0.40 Pain Relevance 0
These results further confirmed that, constitutive and LN-induced FAK phosphorylation was at least partially responsible for the intrinsic chemoresistance to Gem in pancreatic cancer cells.


LN Positive_regulation (induced) of Phosphorylation (phosphorylation) of FAK associated with pancreatic cancer
4) Confidence 0.03 Published 2009 Journal Mol Cancer Section Body Doc Link PMC2806309 Disease Relevance 0.67 Pain Relevance 0
In conclusion, our research demonstrates for the first time that both constitutive and LN-induced FAK phosphorylation contribute to increased intrinsic chemoresistance to Gem in pancreatic cancer cell lines and these effects are partly due to the regulation of Akt and Bad phosphorylation and survivin expression.
LN Positive_regulation (induced) of Phosphorylation (phosphorylation) of FAK associated with pancreatic cancer
5) Confidence 0.03 Published 2009 Journal Mol Cancer Section Abstract Doc Link PMC2806309 Disease Relevance 0.44 Pain Relevance 0
We further found that laminin (LN) induced FAK and Akt phosphorylation in a time-dependent manner, increased the levels of survivin and pBad (pS136) and decreased Gem-induced cytotoxicity and apoptosis in AsPC-1 cells; Specific inhibition of LN-induced FAK phosphorylation by either FAK RNAi or FRNK overexpression suppressed the effects of LN on AsPC-1 cells.
LN Positive_regulation (induced) of Phosphorylation (phosphorylation) of FAK in AsPC-1 associated with apoptosis
6) Confidence 0.03 Published 2009 Journal Mol Cancer Section Abstract Doc Link PMC2806309 Disease Relevance 0.65 Pain Relevance 0
We further found that laminin (LN) induced FAK and Akt phosphorylation in a time-dependent manner, increased the levels of survivin and pBad (pS136) and decreased Gem-induced cytotoxicity and apoptosis in AsPC-1 cells; Specific inhibition of LN-induced FAK phosphorylation by either FAK RNAi or FRNK overexpression suppressed the effects of LN on AsPC-1 cells.
LN Positive_regulation (induced) of Phosphorylation (phosphorylation) of FAK in AsPC-1 associated with apoptosis
7) Confidence 0.03 Published 2009 Journal Mol Cancer Section Abstract Doc Link PMC2806309 Disease Relevance 0.70 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.
LN Positive_regulation (induced) of Phosphorylation (phosphorylation) of FAK
8) Confidence 0.03 Published 2009 Journal Mol Cancer Section Body Doc Link PMC2806309 Disease Relevance 0.68 Pain Relevance 0
Our research demonstrates for the first time that both constitutive and LN-induced phosphorylation of FAK contribute to the intrinsic chemoresistance to Gem in pancreatic cancer cell lines.
LN Positive_regulation (induced) of Phosphorylation (phosphorylation) of FAK associated with pancreatic cancer
9) Confidence 0.03 Published 2009 Journal Mol Cancer Section Body Doc Link PMC2806309 Disease Relevance 0.96 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.
LN Positive_regulation (stimulation) of Phosphorylation (phosphorylation) of FAK in AsPC-1
10) Confidence 0.03 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

LN Positive_regulation (induced) of Phosphorylation (phosphorylation) of FAK in AsPC-1 associated with pancreatic cancer and apoptosis
11) Confidence 0.03 Published 2009 Journal Mol Cancer Section Body Doc Link PMC2806309 Disease Relevance 0.52 Pain Relevance 0
Moreover, inhibition of constitutive FAK phosphorylation in Panc-1 cells and LN-induced FAK phosphorylation in AsPC-1 cells by a novel and more specific FAK phosphorylation inhibitor PF-573,228 showed similar results with those of FAK phosphorylation inhibition by FAK RNAi or FRNK overexpression.


LN Positive_regulation (induced) of Phosphorylation (phosphorylation) of FAK in AsPC-1
12) Confidence 0.03 Published 2009 Journal Mol Cancer Section Abstract Doc Link PMC2806309 Disease Relevance 0.56 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.
LN Positive_regulation (induced) of Phosphorylation (phosphorylation) of FAK
13) Confidence 0.03 Published 2009 Journal Mol Cancer Section Body Doc Link PMC2806309 Disease Relevance 0.37 Pain Relevance 0

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