INT39560

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Context Info
Confidence 0.67
First Reported 1985
Last Reported 2010
Negated 0
Speculated 0
Reported most in Body
Documents 25
Total Number 26
Disease Relevance 10.67
Pain Relevance 2.50

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

peptidase activity (F10) extracellular region (F10) plasma membrane (F10)
Anatomy Link Frequency
platelet 3
blood 2
plasma 2
endothelial cell 1
liver 1
F10 (Homo sapiens)
Pain Link Frequency Relevance Heat
Angina 14 98.84 Very High Very High Very High
Bioavailability 14 98.50 Very High Very High Very High
Inflammation 177 98.12 Very High Very High Very High
aspirin 26 89.68 High High
abdominal pain 2 86.64 High High
palliative 1 86.56 High High
ischemia 22 85.44 High High
cva 139 80.64 Quite High
cytokine 156 76.96 Quite High
antagonist 26 70.08 Quite High
Disease Link Frequency Relevance Heat
Pressure And Volume Under Development 7 98.96 Very High Very High Very High
Cv General 3 Under Development 74 98.84 Very High Very High Very High
Thrombosis 284 98.72 Very High Very High Very High
Cirrhosis 1 98.64 Very High Very High Very High
INFLAMMATION 193 98.12 Very High Very High Very High
Coagulation Disorder 19 97.32 Very High Very High Very High
Disseminated Intravascular Coagulation 12 96.80 Very High Very High Very High
Malignant Neoplastic Disease 3 93.04 High High
Hemorrhage 67 90.48 High High
Syndrome 16 88.48 High High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
The activation of factor X was stopped after 30 minutes by the addition of 35 ?
Positive_regulation (activation) of factor X
1) Confidence 0.67 Published 2003 Journal Thromb J Section Body Doc Link PMC179879 Disease Relevance 0 Pain Relevance 0
One hour after intervention, an increase of plasma TF and TFPI/FXa was seen in both treatment groups.
Positive_regulation (increase) of FXa in plasma
2) Confidence 0.67 Published 2003 Journal Blood Coagul. Fibrinolysis Section Abstract Doc Link 12945880 Disease Relevance 0.41 Pain Relevance 0.47
At baseline, significantly higher levels of plasma TF and TFPI/FXa were found in patients with unstable angina [TF, 161 pg/ml (126-191 pg/ml); TFPI/FXa, 7.8 ng/ml (6.1-9.6 ng/ml)] compared with stable angina [TF, 62 pg/ml (46-82 pg/ml), P < 0.0001; TFPI/FXa, 4.5 ng/ml (3-7.6 ng/ml), P= 0.003].
Positive_regulation (levels) of FXa in plasma associated with angina
3) Confidence 0.67 Published 2003 Journal Blood Coagul. Fibrinolysis Section Abstract Doc Link 12945880 Disease Relevance 0.42 Pain Relevance 0.46
Activation of factor X to FXa initiates the conversion of prothrombin to thrombin which leads to conversion of fibrinogen to fibrin and eventually clot formation (Figure 1).
Positive_regulation (Activation) of factor X
4) Confidence 0.54 Published 2008 Journal Vascular Health and Risk Management Section Body Doc Link PMC2597756 Disease Relevance 0.08 Pain Relevance 0.03
In contrast to unfractionated heparin (UFH), LMWH have greater bioavailability, a more predictable anticoagulant response, longer half-life and a higher proportion of anti-factor Xa to anti-factor IIa activity.
Positive_regulation (proportion) of factor Xa associated with bioavailability
5) Confidence 0.49 Published 2005 Journal Expert Opin Pharmacother Section Abstract Doc Link 15957976 Disease Relevance 0.32 Pain Relevance 0.13
Platelet aggregation or Factor X activation by ascitic fluid and failure of the liver to inactivate activated clotting factors may play a role in this coagulopathy.
Positive_regulation (activation) of Factor X in liver associated with coagulation disorder
6) Confidence 0.46 Published 1985 Journal Cancer Section Abstract Doc Link 3995480 Disease Relevance 1.96 Pain Relevance 0.17
Elevated levels of activated coagulation factor XIIa during CPB supported this theory [4].
Positive_regulation (activated) of factor X
7) Confidence 0.45 Published 2003 Journal Thromb J Section Body Doc Link PMC179879 Disease Relevance 0 Pain Relevance 0
Together (TF/FVIIa) they activate Factor X (FX) and Factor IX (FIX) and start the extrinsic pathway of blood coagulation.
Positive_regulation (activate) of Factor X in blood
8) Confidence 0.42 Published 2006 Journal Thromb. Res. Section Abstract Doc Link 16378835 Disease Relevance 0.80 Pain Relevance 0.18
Together (TF/FVIIa) they activate Factor X (FX) and Factor IX (FIX) and start the extrinsic pathway of blood coagulation.
Positive_regulation (activate) of FX in blood
9) Confidence 0.42 Published 2006 Journal Thromb. Res. Section Abstract Doc Link 16378835 Disease Relevance 0.80 Pain Relevance 0.19
Activation of factor X to FXa initiates the conversion of prothrombin to thrombin which leads to conversion of fibrinogen to fibrin and eventually clot formation (Figure 1).
Positive_regulation (Activation) of FXa
10) Confidence 0.39 Published 2008 Journal Vascular Health and Risk Management Section Body Doc Link PMC2597756 Disease Relevance 0.08 Pain Relevance 0.03
Additionally, activated Factor X (Factor Xa) can mediate signal transduction via specific binding to annexin 2 [67].
Positive_regulation (activated) of Factor X
11) Confidence 0.39 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2793011 Disease Relevance 0.95 Pain Relevance 0.04
We sought to determine where activated factor X (FXa), (pro)thrombin, and fibrin(ogen) are localized in thrombi formed under venous shear.


Positive_regulation (activated) of factor X
12) Confidence 0.35 Published 2010 Journal PLoS ONE Section Abstract Doc Link PMC2861630 Disease Relevance 0.05 Pain Relevance 0
We sought to determine where activated factor X (FXa), (pro)thrombin, and fibrin(ogen) are localized in thrombi formed under venous shear.


Positive_regulation (activated) of FXa
13) Confidence 0.35 Published 2010 Journal PLoS ONE Section Abstract Doc Link PMC2861630 Disease Relevance 0.05 Pain Relevance 0
On the contrary, direct FXa inhibitors, including rivaroxaban, do not need AT to exert their inhibitory action on FXa, because they are able to bind directly to the active site of FXa, thereby preventing interaction with its substrates.
Positive_regulation (action) of FXa
14) Confidence 0.34 Published 2008 Journal Vascular Health and Risk Management Section Body Doc Link PMC2597756 Disease Relevance 0 Pain Relevance 0
PS provides a binding surface for the assembly of the coagulation tenase and prothrombinase complexes, which convert factor X into activated factor X (FXa) and prothrombin into thrombin, respectively [10], [11].
Positive_regulation (activated) of factor X
15) Confidence 0.32 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2861630 Disease Relevance 0.32 Pain Relevance 0.03
PS provides a binding surface for the assembly of the coagulation tenase and prothrombinase complexes, which convert factor X into activated factor X (FXa) and prothrombin into thrombin, respectively [10], [11].
Positive_regulation (activated) of factor X
16) Confidence 0.32 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2861630 Disease Relevance 0.32 Pain Relevance 0.03
PS provides a binding surface for the assembly of the coagulation tenase and prothrombinase complexes, which convert factor X into activated factor X (FXa) and prothrombin into thrombin, respectively [10], [11].
Positive_regulation (activated) of FXa
17) Confidence 0.32 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2861630 Disease Relevance 0.32 Pain Relevance 0.03
Not surprisingly, since FXa is the key coagulation factor lying at the crossroads of intrinsic and extrinsic coagulation, a significant interest exists in developing drugs which specifically target activated FXa.
Positive_regulation (activated) of FXa
18) Confidence 0.32 Published 2010 Journal Vascular Health and Risk Management Section Body Doc Link PMC2879296 Disease Relevance 0.49 Pain Relevance 0.13
In parallel with our in vitro studies, a punctate distribution of FXa was observed, in accord with the notion that FXa binding is localized to the platelet surface during thrombus formation.
Positive_regulation (distribution) of FXa in platelet associated with thrombosis
19) Confidence 0.30 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2861630 Disease Relevance 0.40 Pain Relevance 0
Fluorescence microscopy was used to study the accumulation of platelets, FXa, (pro)thrombin, and fibrin(ogen) in thrombi formed in vitro and in vivo.
Positive_regulation (accumulation) of FXa in platelets
20) Confidence 0.28 Published 2010 Journal PLoS ONE Section Abstract Doc Link PMC2861630 Disease Relevance 0.13 Pain Relevance 0

General Comments

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