INT11481

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Context Info
Confidence 0.58
First Reported 1987
Last Reported 2010
Negated 0
Speculated 0
Reported most in Body
Documents 11
Total Number 11
Disease Relevance 5.53
Pain Relevance 1.80

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 (F12) extracellular space (F12) extracellular region (F12)
plasma membrane (F12)
Anatomy Link Frequency
plasma 3
endothelial cells 1
cleavage 1
F12 (Homo sapiens)
Pain Link Frequency Relevance Heat
bradykinin 78 99.92 Very High Very High Very High
rheumatoid arthritis 3 94.72 High High
Pain 28 93.56 High High
b2 receptor 9 87.32 High High
Osteoarthritis 1 61.76 Quite High
backache 1 61.00 Quite High
Inflammation 5 51.84 Quite High
Antihistamine 11 34.32 Quite Low
antagonist 20 32.52 Quite Low
abdominal pain 11 5.00 Very Low Very Low Very Low
Disease Link Frequency Relevance Heat
Hereditary Angioedema 409 98.44 Very High Very High Very High
Angioedema 22 97.40 Very High Very High Very High
Disease 49 97.08 Very High Very High Very High
Hypersensitivity 21 95.20 Very High Very High Very High
Pain 21 93.56 High High
Pressure Volume 2 Under Development 6 93.24 High High
Congenital Anomalies 2 92.00 High High
Edema 51 91.92 High High
Pressure And Volume Under Development 152 91.64 High High
Pox Virus Infection 3 89.80 High High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
Experiments using purified enzyme of the K-K cascade indicated that Neurotropin inhibited surface-mediated activation of coagulation factor XII (FXII) and the activation of prekallikrein by FXIIa.
Positive_regulation (activation) of coagulation factor XII
1) Confidence 0.58 Published 1992 Journal Biochem. Pharmacol. Section Abstract Doc Link 1562287 Disease Relevance 0.46 Pain Relevance 0.30
It was hypothesized that an abnormal coagulation factor XII molecule may lead to inappropriate activation of the kinin-forming cascade of which factor XII is a major constituent.
Positive_regulation (activation) of factor XII
2) Confidence 0.46 Published 2010 Journal Allergy Asthma Clin Immunol Section Body Doc Link PMC2919521 Disease Relevance 0.43 Pain Relevance 0
Effect of neurotropin on the binding of high molecular weight kininogen and Hageman factor to human umbilical vein endothelial cells and the autoactivation of bound Hageman factor.
Positive_regulation (autoactivation) of Hageman factor in endothelial cells
3) Confidence 0.42 Published 1998 Journal Biochem. Pharmacol. Section Title Doc Link 9719471 Disease Relevance 0.28 Pain Relevance 0.23
In dextran sulfate-activated plasma, Neurotropin inhibited the formation of BK, the cleavage of high molecular weight kininogen (HK) and the formation of kallikrein-C1 inhibitor and activated coagulation factor XII (FXIIa)-C1 inhibitor complexes.
Positive_regulation (activated) of coagulation factor XII in cleavage associated with bradykinin
4) Confidence 0.39 Published 1992 Journal Biochem. Pharmacol. Section Abstract Doc Link 1562287 Disease Relevance 0.44 Pain Relevance 0.30
Recent studies have revealed that microbial and human cell proteinases activate Hageman factor and/or prekallikrein, or directly release kinin from kininogens.
Positive_regulation (activate) of Hageman factor
5) Confidence 0.10 Published 2004 Journal Biol. Chem. Section Abstract Doc Link 15576318 Disease Relevance 0.50 Pain Relevance 0.09
Kinins are released from kininogens through the activation of the Hageman factor-prekallikrein system or by tissue kallikrein.
Positive_regulation (activation) of Hageman factor
6) Confidence 0.09 Published 2004 Journal Biol. Chem. Section Abstract Doc Link 15576318 Disease Relevance 0.25 Pain Relevance 0.09
However, the ability of the solid-phase assay to detect and quantitate alpha 2M-proteinase complexes when they are present was confirmed in control experiments with plasma samples to which performed alpha 2M-trypsin complexes had been added, or in which alpha 2M-kallikrein complexes had been generated by activation of Hageman factor (coagulation factor XII).
Positive_regulation (activation) of coagulation factor XII in plasma
7) Confidence 0.09 Published 1987 Journal Arthritis Rheum. Section Abstract Doc Link 2443146 Disease Relevance 0.26 Pain Relevance 0.21
Cugno and colleagues have speculated that the significant increases in prothrombin fragment F1+2 in the coagulation pathway may involve increased plasma levels of factor XII, an initiator of the contact pathway that is activated during HAE attacks [18].
Positive_regulation (increased) of factor XII in plasma associated with hereditary angioedema
8) Confidence 0.04 Published 2008 Journal Clin Mol Allergy Section Body Doc Link PMC2374835 Disease Relevance 0.58 Pain Relevance 0.11
C1-inhibitor replacement therapy not only suppresses bradykinin release by inactivation of factor XIIa and kallikrein, but also suppresses activation of the complement system and perhaps of the fibrinolytic and coagulation pathways.
Positive_regulation (inactivation) of factor XIIa associated with bradykinin
9) Confidence 0.03 Published 2008 Journal Clin Mol Allergy Section Body Doc Link PMC2374835 Disease Relevance 0.19 Pain Relevance 0.05
Inherited C1 inhibitor deficiency with normal C1 inhibitor activity (formerly HAE type 3) is a very rare disorder seen primarily in women and may be caused by increased activity of factor XII within the contact pathway, leading to increased bradykinin and angioedema[2,9].
Positive_regulation (increased) of factor XII associated with hereditary angioedema, angioedema and bradykinin
10) Confidence 0.02 Published 2010 Journal BMC Blood Disord Section Body Doc Link PMC2881905 Disease Relevance 1.09 Pain Relevance 0.12
Replacement therapy with C1INH will inhibit both plasma kallikrein and activated factor XII.
Positive_regulation (activated) of factor XII in plasma
11) Confidence 0.01 Published 2010 Journal Allergy Asthma Clin Immunol Section Body Doc Link PMC2921104 Disease Relevance 1.06 Pain Relevance 0.30

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