INT142066

From wiki-pain
Jump to: navigation, search
Context Info
Confidence 0.48
First Reported 2007
Last Reported 2008
Negated 1
Speculated 0
Reported most in Body
Documents 5
Total Number 21
Disease Relevance 0.24
Pain Relevance 3.73

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

plasma membrane (CFL1) cytoskeleton (CFL1) nucleus (CFL1)
intracellular (CFL1) cytoskeleton organization (CFL1) cytoplasm (CFL1)
Anatomy Link Frequency
intestinal cells 2
CFL1 (Homo sapiens)
Pain Link Frequency Relevance Heat
qutenza 40 99.98 Very High Very High Very High
agonist 221 99.62 Very High Very High Very High
Angina 17 9.00 Low Low
imagery 34 5.00 Very Low Very Low Very Low
antagonist 17 5.00 Very Low Very Low Very Low
Disease Link Frequency Relevance Heat
Leukemia 17 77.12 Quite High
Targeted Disruption 68 60.84 Quite High
Stress 51 53.44 Quite High
Disease 34 32.44 Quite Low
Coronary Artery Disease 17 12.60 Low Low
Hypertension 68 11.52 Low Low
Atherosclerosis 51 9.68 Low Low
Cv General 3 Under Development 17 9.00 Low Low
Myocardial Infarction 17 8.32 Low Low
Thrombosis 51 7.40 Low Low

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
Our data suggest that TJ opening is mediated by cofilin dephosphorylation, which is caused by capsaicin stimuli, including Ca2+ influx.
Positive_regulation (mediated) of Phosphorylation (dephosphorylation) of cofilin associated with qutenza
1) Confidence 0.48 Published 2007 Journal Biochem. Biophys. Res. Commun. Section Abstract Doc Link 17303079 Disease Relevance 0 Pain Relevance 0.74
The Ca2+-chelating reagent EGTA blocked the cofilin dephosphorylation induced by both capsaicin and ionomycin, suggesting that the dephosphorylation was mediated by Ca2+ influx.
Positive_regulation (induced) of Phosphorylation (dephosphorylation) of cofilin associated with qutenza
2) Confidence 0.48 Published 2007 Journal Biochem. Biophys. Res. Commun. Section Abstract Doc Link 17303079 Disease Relevance 0 Pain Relevance 0.76
Capsaicin induces cofilin dephosphorylation in human intestinal cells: the triggering role of cofilin in tight-junction signaling.
Positive_regulation (induces) of Phosphorylation (dephosphorylation) of cofilin in intestinal cells associated with qutenza
3) Confidence 0.48 Published 2007 Journal Biochem. Biophys. Res. Commun. Section Title Doc Link 17303079 Disease Relevance 0 Pain Relevance 0.83
Our data suggest that TJ opening is mediated by cofilin dephosphorylation, which is caused by capsaicin stimuli, including Ca2+ influx.
Positive_regulation (caused) of Phosphorylation (dephosphorylation) of cofilin associated with qutenza
4) Confidence 0.48 Published 2007 Journal Biochem. Biophys. Res. Commun. Section Abstract Doc Link 17303079 Disease Relevance 0 Pain Relevance 0.74
activation to mobilize Ca2+ from IP3-operated intracellular stores, for example, and to G12-dependent RhoA activation and effector coupling leading to cofilin phosphorylation and inactivation and to F-actin polymerization.


Positive_regulation (leading) of Phosphorylation (phosphorylation) of cofilin
5) Confidence 0.22 Published 2008 Journal Cellular Signalling Section Body Doc Link PMC2681257 Disease Relevance 0.05 Pain Relevance 0
Similarly, while the NO donors SIN-1 and FK409 alone did not induce substantial RhoA signaling relative to the drug vehicle per se, they each significantly impaired U46619-induced RhoA activation and cofilin phosphorylation following their pre-incubation in 1° h.AoSMCs (Fig. 7B and D).
Positive_regulation (following) of Phosphorylation (phosphorylation) of cofilin
6) Confidence 0.22 Published 2008 Journal Cellular Signalling Section Body Doc Link PMC2681257 Disease Relevance 0 Pain Relevance 0.08
Stimulation of 1° h.AoSMCs also led to rapid F-actin polymerization (Fig. 6B) and cofilin phosphorylation with optimal responses generated using 1 ?
Positive_regulation (led) of Phosphorylation (phosphorylation) of cofilin
7) Confidence 0.22 Published 2008 Journal Cellular Signalling Section Body Doc Link PMC2681257 Disease Relevance 0 Pain Relevance 0.11
Moreover, U46619-induced cofilin phosphorylation by TP?
Positive_regulation (by) of Phosphorylation (phosphorylation) of cofilin
8) Confidence 0.16 Published 2008 Journal Cellular Signalling Section Body Doc Link PMC2681257 Disease Relevance 0 Pain Relevance 0
Similarly, to assess U46619-mediated cofilin phosphorylation and activation, aliquots of whole cells lysates (typically 10 ?
Positive_regulation (mediated) of Phosphorylation (phosphorylation) of cofilin
9) Confidence 0.16 Published 2008 Journal Cellular Signalling Section Body Doc Link PMC2681257 Disease Relevance 0 Pain Relevance 0.03
Similarly, to assess U46619-mediated cofilin phosphorylation and activation, aliquots of whole cells lysates (typically 10 ?
Positive_regulation (activation) of Phosphorylation (phosphorylation) of cofilin
10) Confidence 0.16 Published 2008 Journal Cellular Signalling Section Body Doc Link PMC2681257 Disease Relevance 0 Pain Relevance 0.03
-mediated RhoA activation, F-actin polymerization and cofilin phosphorylation was also specifically impaired by Cicaprost and SIN-1 while neither agent affected Rho-mediated signaling by TP?.
Positive_regulation (mediated) of Phosphorylation (phosphorylation) of cofilin
11) Confidence 0.16 Published 2008 Journal Cellular Signalling Section Body Doc Link PMC2681257 Disease Relevance 0.05 Pain Relevance 0
led to a further significant reduction in U46619-induced Rho activation and cofilin phosphorylation.
Positive_regulation (activation) of Phosphorylation (phosphorylation) of cofilin
12) Confidence 0.16 Published 2008 Journal Cellular Signalling Section Body Doc Link PMC2681257 Disease Relevance 0 Pain Relevance 0
Consistent with this, the specific PGD2 receptor (DP) agonist BW245C also significantly impaired RhoA activation (Fig. 7C) and cofilin phosphorylation in 1° h.AoSMCs.
Positive_regulation (activation) of Phosphorylation (phosphorylation) of cofilin associated with agonist
13) Confidence 0.16 Published 2008 Journal Cellular Signalling Section Body Doc Link PMC2681257 Disease Relevance 0 Pain Relevance 0.09
While the IP agonist Cicaprost did not lead to substantial RhoA activation and cofilin phosphorylation relative to the drug vehicle per se, it significantly impaired such U46619-mediated signaling in 1° h.AoSMCs (Fig. 7A).
Positive_regulation (activation) of Phosphorylation (phosphorylation) of cofilin associated with agonist
14) Confidence 0.16 Published 2008 Journal Cellular Signalling Section Body Doc Link PMC2681257 Disease Relevance 0 Pain Relevance 0.09
expressed in HEK 293 cells readily induced RhoA activation, F-actin polymerization and cofilin phosphorylation in response to U46619.
Positive_regulation (activation) of Phosphorylation (phosphorylation) of cofilin
15) Confidence 0.16 Published 2008 Journal Cellular Signalling Section Body Doc Link PMC2681257 Disease Relevance 0.08 Pain Relevance 0.04
While the IP agonist Cicaprost did not lead to substantial RhoA activation and cofilin phosphorylation relative to the drug vehicle per se, it significantly impaired such U46619-mediated signaling in 1° h.AoSMCs (Fig. 7A).
Neg (not) Positive_regulation (lead) of Phosphorylation (phosphorylation) of cofilin associated with agonist
16) Confidence 0.16 Published 2008 Journal Cellular Signalling Section Body Doc Link PMC2681257 Disease Relevance 0 Pain Relevance 0.09
Consistent with their reduced expression in the 1° h.AoSMCs, there was a significant reduction in U46619-mediated Rho activation and cofilin phosphorylation in the presence of RNAi directed to either TP?
Positive_regulation (activation) of Phosphorylation (phosphorylation) of cofilin
17) Confidence 0.16 Published 2008 Journal Cellular Signalling Section Body Doc Link PMC2681257 Disease Relevance 0.06 Pain Relevance 0
both SIN-1 and Cicaprost reduced U46619-mediated RhoA, F-actin polymerization (data not shown) and cofilin phosphorylation to levels not significantly different to those observed in vehicle-treated cells.
Positive_regulation (mediated) of Phosphorylation (phosphorylation) of cofilin
18) Confidence 0.16 Published 2008 Journal Cellular Signalling Section Body Doc Link PMC2681257 Disease Relevance 0 Pain Relevance 0
following incubation of the 1° h.AoSMCs with the isoform-specific siRNAs, there were reductions in U46619-induced Rho activation and cofilin phosphorylation in the presence of RNAi directed to either TP but not directed to Lamin A/C (Fig. 9B).
Positive_regulation (activation) of Phosphorylation (phosphorylation) of cofilin
19) Confidence 0.16 Published 2008 Journal Cellular Signalling Section Body Doc Link PMC2681257 Disease Relevance 0 Pain Relevance 0
Moreover, Cicaprost (IP agonist) and BW245C (DP agonist) and the NO donors SIN-1 and FK409 each significantly impaired such U46619-induced RhoA activation, F-actin polymerization and cofilin phosphorylation in 1° h.AoSMCs.
Positive_regulation (activation) of Phosphorylation (phosphorylation) of cofilin associated with agonist
20) Confidence 0.16 Published 2008 Journal Cellular Signalling Section Body Doc Link PMC2681257 Disease Relevance 0 Pain Relevance 0.10

General Comments

This test has worked.

Personal tools
Namespaces

Variants
Actions
Navigation
Toolbox