INT184378

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Context Info
Confidence 0.20
First Reported 2005
Last Reported 2009
Negated 2
Speculated 1
Reported most in Body
Documents 54
Total Number 55
Disease Relevance 12.49
Pain Relevance 2.36

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

cell proliferation (Cfb) peptidase activity (Cfb) extracellular space (Cfb)
extracellular region (Cfb)
Anatomy Link Frequency
cleavage 3
Iris 3
plasma 2
blood 1
neutrophils 1
Cfb (Mus musculus)
Pain Link Frequency Relevance Heat
rheumatoid arthritis 468 98.68 Very High Very High Very High
Inflammation 583 98.44 Very High Very High Very High
Arthritis 123 97.68 Very High Very High Very High
cva 63 89.76 High High
cytokine 34 83.84 Quite High
ischemia 153 83.08 Quite High
antagonist 45 80.36 Quite High
Multiple sclerosis 43 66.68 Quite High
psoriasis 43 65.88 Quite High
alcohol 6 63.04 Quite High
Disease Link Frequency Relevance Heat
Targeted Disruption 124 99.80 Very High Very High Very High
Age-related Macular Degeneration 147 99.60 Very High Very High Very High
Herpes Simplex Virus 43 99.38 Very High Very High Very High
Rheumatoid Arthritis 468 98.68 Very High Very High Very High
INFLAMMATION 687 98.44 Very High Very High Very High
Arthritis 130 97.68 Very High Very High Very High
Paroxysmal Nocturnal Hemoglobinuria 97 96.28 Very High Very High Very High
Disease Progression 5 95.84 Very High Very High Very High
American Trypanosomiasis 43 95.68 Very High Very High Very High
Injury 174 93.12 High High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
An independent study further established a similar association between CFB, C2, and AMD [85].
CFB Binding (association) of associated with age-related macular degeneration
1) Confidence 0.20 Published 2008 Journal Semin Immunopathol Section Body Doc Link PMC2315691 Disease Relevance 1.03 Pain Relevance 0.06
It also competes with factor B for surface-bound C3b [26].
factor B Binding (competes) of
2) Confidence 0.17 Published 2008 Journal Semin Immunopathol Section Body Doc Link PMC2315691 Disease Relevance 0 Pain Relevance 0
As expected, ACPA+ sera showed reactivity to CFb but not to unmodified Fb (Figure 4A, lanes 1 and 2), whilst no reactivity was observed with ACPA?
CFb Neg (not) Binding (reactivity) of
3) Confidence 0.16 Published 2009 Journal PLoS Medicine Section Body Doc Link PMC2621263 Disease Relevance 0.10 Pain Relevance 0.05
It acts via three mechanisms: preventing the formation of the C3 convertase by binding to C4b; accelerating the natural decay of the classical pathway C3 convertase; and as a cofactor for the serine proteinase factor I in the proteolytic inactivation of C4b, which prevents the formation of the C3 convertase.
convertase Binding (formation) of
4) Confidence 0.07 Published 2007 Journal Arthritis Res Ther Section Body Doc Link PMC2212569 Disease Relevance 0.37 Pain Relevance 0.07
It acts via three mechanisms: preventing the formation of the C3 convertase by binding to C4b; accelerating the natural decay of the classical pathway C3 convertase; and as a cofactor for the serine proteinase factor I in the proteolytic inactivation of C4b, which prevents the formation of the C3 convertase.
convertase Binding (formation) of
5) Confidence 0.07 Published 2007 Journal Arthritis Res Ther Section Body Doc Link PMC2212569 Disease Relevance 0.53 Pain Relevance 0.07
The chemotactic effects of C5a-C5aR ligation then attracts neutrophils to sites of inflammation to produce properdin, which, upon binding to C3b-IgG complexes, enhances the association with factor B, leading to stabilization of the alternative pathway C3 convertase and amplification of the alternative pathway C3 consumption.
factor B Binding (association) of in neutrophils associated with inflammation
6) Confidence 0.07 Published 2005 Journal Arthritis Res Ther Section Body Doc Link PMC1175042 Disease Relevance 0.70 Pain Relevance 0.25
We concluded that I. ricinus IxACs specifically interacted with properdin and prevented its binding to C3b.
properdin Binding (interacted) of
7) Confidence 0.06 Published 2008 Journal PLoS ONE Section Body Doc Link PMC2151134 Disease Relevance 0 Pain Relevance 0
Nevertheless, it remains to be seen whether IxACs can also interfere with the binding of properdin to the target surface.
properdin Binding (binding) of
8) Confidence 0.06 Published 2008 Journal PLoS ONE Section Body Doc Link PMC2151134 Disease Relevance 0.45 Pain Relevance 0.11
Overall, these results show that I. ricinus IxAC proteins inhibit the formation of the C3 convertase complex by interacting specifically with properdin.
properdin Binding (interacting) of
9) Confidence 0.06 Published 2008 Journal PLoS ONE Section Body Doc Link PMC2151134 Disease Relevance 0 Pain Relevance 0
This is reminiscent of the effect of monoclonal antibodies that bind to properdin and knock out of the properdin gene in mice, and both lead to inhibition of the AP [19].To our knowledge this is the first time that direct interaction with properdin is described as a mechanism of complement regulation.
properdin Binding (interaction) of associated with targeted disruption
10) Confidence 0.06 Published 2008 Journal PLoS ONE Section Body Doc Link PMC2151134 Disease Relevance 0.10 Pain Relevance 0
I. ricinus IxACs specifically interact with properdin
properdin Binding (interact) of
11) Confidence 0.06 Published 2008 Journal PLoS ONE Section Body Doc Link PMC2151134 Disease Relevance 0 Pain Relevance 0
Properdin binds to surface-bound C3b and increases its ability to interact with factor B [17].
Properdin Binding (binds) of
12) Confidence 0.06 Published 2008 Journal PLoS ONE Section Body Doc Link PMC2151134 Disease Relevance 0 Pain Relevance 0
Two recent reports further emphasize the importance of properdin in the AP: Spitzer et al. [52] and Kimura et al. [53] showed that properdin can also bind directly to microbes, initiating assembly of C3BbP convertase and complement activation.
properdin Binding (bind) of
13) Confidence 0.06 Published 2008 Journal PLoS ONE Section Body Doc Link PMC2151134 Disease Relevance 0.22 Pain Relevance 0.03
Indeed although the general 3D structure of IxACs appears to have been conserved, small changes might modulate their interaction with properdin.
properdin Spec (might) Binding (interaction) of
14) Confidence 0.06 Published 2008 Journal PLoS ONE Section Body Doc Link PMC2151134 Disease Relevance 0 Pain Relevance 0
Increasing amounts of IRAC II, IxAC-B1 but not Iris lead to a decrease in the amount of bound properdin.
properdin Binding (bound) of in Iris
15) Confidence 0.06 Published 2008 Journal PLoS ONE Section Body Doc Link PMC2151134 Disease Relevance 0 Pain Relevance 0
However, progeny mice of crosses between K/B × N and knockout mice deficient for either complement factor B, C3, C5 or C5aR were found to be completely resistant to arthritis.
factor B Binding (complement) of associated with targeted disruption and arthritis
16) Confidence 0.06 Published 2005 Journal Arthritis Res Ther Section Body Doc Link PMC1175042 Disease Relevance 1.26 Pain Relevance 0.32
They all inhibited formation of C3 convertase by specifically binding to properdin.
convertase Binding (formation) of
17) Confidence 0.05 Published 2008 Journal PLoS ONE Section Body Doc Link PMC2151134 Disease Relevance 0.18 Pain Relevance 0
Although they were able to stop the ongoing formation of C3 convertase they could not undo previously formed complexes.
convertase Binding (formation) of
18) Confidence 0.05 Published 2008 Journal PLoS ONE Section Body Doc Link PMC2151134 Disease Relevance 0 Pain Relevance 0
Surface protein gC of Herpes Simplex Virus binds to C3b and inhibits its association with C5 and properdin [59].
properdin Binding (association) of associated with herpes simplex virus
19) Confidence 0.05 Published 2008 Journal PLoS ONE Section Body Doc Link PMC2151134 Disease Relevance 0.29 Pain Relevance 0
Because there are no complement regulatory proteins – which usually inhibit complement activation on eukaryotic cells – present on the cartilage surface and because the bound IgGs are able to bind C3b and prevent the binding of the complement regulatory plasma proteins factor I and factor H, formation of the C3 convertase is possible.
convertase Binding (formation) of in plasma
20) Confidence 0.05 Published 2005 Journal Arthritis Res Ther Section Body Doc Link PMC1175042 Disease Relevance 0.76 Pain Relevance 0.21

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