INT181015

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Context Info
Confidence 0.58
First Reported 2005
Last Reported 2010
Negated 1
Speculated 0
Reported most in Body
Documents 12
Total Number 12
Disease Relevance 8.90
Pain Relevance 2.18

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

signal transduction (C3ar1) plasma membrane (C3ar1) signal transducer activity (C3ar1)
Anatomy Link Frequency
leukocytes 1
cleavage 1
Dendritic cells 1
central nervous system 1
T-cells 1
C3ar1 (Mus musculus)
Pain Link Frequency Relevance Heat
Inflammation 292 100.00 Very High Very High Very High
cytokine 117 98.88 Very High Very High Very High
Central nervous system 23 98.72 Very High Very High Very High
chemokine 31 98.32 Very High Very High Very High
ischemia 15 97.28 Very High Very High Very High
Arthritis 46 96.12 Very High Very High Very High
Inflammatory response 49 86.56 High High
Pain 23 84.76 Quite High
depression 1 83.08 Quite High
rheumatoid arthritis 36 74.52 Quite High
Disease Link Frequency Relevance Heat
INFLAMMATION 359 100.00 Very High Very High Very High
Gliosis 2 97.88 Very High Very High Very High
Cv General 4 Under Development 1 97.64 Very High Very High Very High
Arthritis 49 96.12 Very High Very High Very High
Anaphylaxis 1 95.36 Very High Very High Very High
Amyloid Plaque 18 95.24 Very High Very High Very High
Injury 186 94.88 High High
Cancer 218 93.20 High High
Necrosis 14 92.72 High High
Disease 386 90.20 High High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
C3aR is expressed on key mediators of the immune system like neutrophils, basophiles, eosinophiles, mast cells, monocytes/macrophages, dendritic cells, microglia, as well as, non myeloid cells like astrocytes, epithelial cells, smooth muscles cells, and activated T-cells, but, interestingly, not naïve T-cells.
Neg (not) Gene_expression (expressed) of C3aR in T-cells
1) Confidence 0.58 Published 2009 Journal Virol J Section Body Doc Link PMC2789730 Disease Relevance 0.54 Pain Relevance 0.13
Dendritic cells that fail to express C3aR suffer reduced T-cell activation.
Gene_expression (express) of C3aR in Dendritic cells
2) Confidence 0.58 Published 2009 Journal Virol J Section Body Doc Link PMC2789730 Disease Relevance 0.51 Pain Relevance 0.12
Nevertheless, included in this set were GPCRs such as Emr1 (F4/80), C3aR, C5aR, Ccrl2 and Ccr2 that are known to be either macrophage-specific or highly expressed by macrophages [8-12], thus validating our approach.
Gene_expression (expressed) of C3aR in F4/80
3) Confidence 0.57 Published 2008 Journal Immunome Res Section Body Doc Link PMC2394514 Disease Relevance 0 Pain Relevance 0
All three pathways activate C3 by forming an enzyme, the C3 convertase, which cleaves C3 generating the C3a anaphylatoxin and the activation product C3b.
Gene_expression (generating) of C3a
4) Confidence 0.11 Published 2007 Journal Arthritis Res Ther Section Body Doc Link PMC2212569 Disease Relevance 0.90 Pain Relevance 0.11
Similarly the two groups did not differ in the number of cells stained for the complement type 3 receptor CD11b which labels microglia (Supplementary Figures S4C & S4D, t13?
Gene_expression (stained) of complement type 3 receptor in microglia
5) Confidence 0.08 Published 2008 Journal PLoS ONE Section Body Doc Link PMC2396793 Disease Relevance 0.46 Pain Relevance 0.07
The anaphylatoxin C3a is a product of complement network activation via all three initiating pathways.
Gene_expression (product) of C3a
6) Confidence 0.07 Published 2005 Journal Arthritis Res Ther Section Body Doc Link PMC1175042 Disease Relevance 0.99 Pain Relevance 0.42
Also expressed by leukocytes in the early inflammatory cluster are C3, a key component of the classical and alternative complement pathways, and its receptor, C3R.
Gene_expression (expressed) of C3R in leukocytes associated with inflammation
7) Confidence 0.06 Published 2005 Journal Genome Biol Section Body Doc Link PMC549066 Disease Relevance 1.33 Pain Relevance 0.19
A. senticosus has been shown to reduce the expression of cyclo-oxygenase (COX)-2 and complement type 3 receptor (a marker for microglia in the central nervous system) in cerebral ischemia [7] and to inhibit mast cell-dependent anaphylaxis [8].
Gene_expression (expression) of and complement type 3 receptor in central nervous system associated with anaphylaxis, cv general 4 under development, ischemia and central nervous system
8) Confidence 0.04 Published 2007 Journal Arthritis Res Ther Section Body Doc Link PMC2206389 Disease Relevance 1.11 Pain Relevance 0.56
The function of the C3 convertase in all three pathways is to further cleave C3, producing C3a, one of the two major anaphylatoxins of the complement system, and C3b, a potent opsonin.
Gene_expression (producing) of C3a
9) Confidence 0.04 Published 2008 Journal Biologics : Targets & Therapy Section Body Doc Link PMC2727911 Disease Relevance 0.06 Pain Relevance 0.03
These cellular events are accompanied by increased expression of members of the complement pathway (C1q, C3b, C3a, membrane attack complex), cytokines and chemokines (interleukin-1?
Gene_expression (expression) of C3a associated with chemokine and cytokine
10) Confidence 0.03 Published 2010 Journal Frontiers in Aging Neuroscience Section Body Doc Link PMC2912027 Disease Relevance 1.29 Pain Relevance 0.19
This activation stimulates production of C3b, membrane attack complex (MAC) and C3a.
Gene_expression (production) of C3a
11) Confidence 0.03 Published 2010 Journal Frontiers in Aging Neuroscience Section Body Doc Link PMC2912027 Disease Relevance 0.99 Pain Relevance 0.22
All the complement cascades culminate in the central cleavage of C3 and in the generation of its active fragments C3a and C3b.
Gene_expression (generation) of C3a in cleavage
12) Confidence 0.02 Published 2010 Journal The Open Virology Journal Section Body Doc Link PMC2936037 Disease Relevance 0.72 Pain Relevance 0.13

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