INT168637

From wiki-pain
Jump to: navigation, search
Context Info
Confidence 0.58
First Reported 2008
Last Reported 2010
Negated 0
Speculated 0
Reported most in Body
Documents 6
Total Number 12
Disease Relevance 11.67
Pain Relevance 2.41

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 (Cx3cr1) plasma membrane (Cx3cr1) signal transducer activity (Cx3cr1)
Anatomy Link Frequency
Monocyte 3
macrophage 2
spinal 1
blood vessels 1
NK cells 1
Cx3cr1 (Mus musculus)
Pain Link Frequency Relevance Heat
Neuropathic pain 2 99.90 Very High Very High Very High
Inflammation 285 99.48 Very High Very High Very High
chemokine 241 99.16 Very High Very High Very High
Lasting pain 1 95.24 Very High Very High Very High
Multiple sclerosis 23 87.48 High High
Pain 10 86.08 High High
Thermal hyperalgesia 2 75.80 Quite High
antagonist 12 74.24 Quite High
allodynia 3 74.16 Quite High
Sciatic nerve 1 72.48 Quite High
Disease Link Frequency Relevance Heat
Targeted Disruption 113 99.92 Very High Very High Very High
Injury 314 99.90 Very High Very High Very High
Neuropathic Pain 7 99.90 Very High Very High Very High
Multiple Sclerosis 320 99.48 Very High Very High Very High
INFLAMMATION 314 99.48 Very High Very High Very High
Necrosis 16 99.00 Very High Very High Very High
Age-related Macular Degeneration 36 98.76 Very High Very High Very High
Pain 11 95.24 Very High Very High Very High
Vasculitis 1 94.68 High High
Disease 126 86.24 High High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
In contrast, CX3CR1 deficiency exacerbates EAE because regulatory NK cells are not recruited to the inflamed CNS [26].
Negative_regulation (deficiency) of CX3CR1 in NK cells associated with multiple sclerosis
1) Confidence 0.58 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2965160 Disease Relevance 1.15 Pain Relevance 0.15
Monocyte recruitment was little affected by loss of the second CX3CR1 allele (Ccr2RFP/+Cx3cr1GFP/GFP), but was markedly reduced by loss of the second CCR2 allele (Ccr2RFP/RFPCx3cr1GFP/+) (Figure 3B).
Negative_regulation (loss) of CX3CR1 allele in Monocyte
2) Confidence 0.58 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2965160 Disease Relevance 0.31 Pain Relevance 0.03
Reduced inflammatory and neuropathic pain and decreased spinal microglial response in fractalkine receptor (CX3CR1) knockout mice.
Negative_regulation (decreased) of CX3CR1 in spinal associated with targeted disruption, inflammation and neuropathic pain
3) Confidence 0.42 Published 2010 Journal J. Neurochem. Section Title Doc Link 20524966 Disease Relevance 2.03 Pain Relevance 0.99
Interestingly, the absence of CX3CR1 in the Ccr2RFP/+Cx3cr1GFP/GFP mice had little or no effect on the RFP/GFP profile or the number of recruited cells.
Negative_regulation (absence) of Cx3cr1GFP
4) Confidence 0.42 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2965160 Disease Relevance 0.96 Pain Relevance 0.21
Interestingly, the absence of CX3CR1 in the Ccr2RFP/+Cx3cr1GFP/GFP mice had little or no effect on the RFP/GFP profile or the number of recruited cells.
Negative_regulation (absence) of CX3CR1
5) Confidence 0.42 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2965160 Disease Relevance 0.90 Pain Relevance 0.21
Thus, our findings reveal that Ly6Clo/CX3CR1+ monocytes are relatively excluded from the inflamed CNS of mice with EAE, regardless of CCR2 expression.
Negative_regulation (excluded) of CX3CR1 in monocytes associated with multiple sclerosis
6) Confidence 0.42 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2965160 Disease Relevance 0.56 Pain Relevance 0.11
Mice deficient in both CCR2 and CX3CR1 (Ccr2RFP/RFPCx3cr1GFP/GFP mice) were included to probe the interactions between these receptors in EAE.
Negative_regulation (deficient) of CX3CR1 associated with multiple sclerosis
7) Confidence 0.42 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2965160 Disease Relevance 1.16 Pain Relevance 0.14
Furuichi et al. (38) has shown that Cx3cr1 is up-regulated at later stages in renal I/R injury and that Cx3cr1 deficiency attenuates macrophage influx 7 days after renal I/R injury.
Negative_regulation (deficiency) of Cx3cr1 in macrophage associated with injury
8) Confidence 0.39 Published 2010 Journal International Immunology Section Body Doc Link PMC2877810 Disease Relevance 1.00 Pain Relevance 0.06
In contrast, Oh et al. (21) concluded that early ischemic acute tubular necrosis (ATN) is partially a Cx3cr1-dependent process as serum creatinine, ATN score and macrophage infiltration are reduced by Cx3cr1 inhibition at early stages of post-ischemic reperfusion.
Negative_regulation (inhibition) of Cx3cr1 in macrophage associated with necrosis
9) Confidence 0.39 Published 2010 Journal International Immunology Section Body Doc Link PMC2877810 Disease Relevance 0.97 Pain Relevance 0.06
Fractalkine expression is increased in the endothelium of large blood vessels, capillaries, and glomeruli in ischemic AKI and fractalkine receptor inhibition is protective against ischemic AKI [60].
Negative_regulation (inhibition) of fractalkine receptor in blood vessels associated with injury
10) Confidence 0.29 Published 2009 Journal Mediators of Inflammation Section Body Doc Link PMC2825552 Disease Relevance 1.02 Pain Relevance 0.27
Monocyte recruitment was little affected by loss of the second CX3CR1 allele (Ccr2RFP/+Cx3cr1GFP/GFP), but was markedly reduced by loss of the second CCR2 allele (Ccr2RFP/RFPCx3cr1GFP/+) (Figure 3B).
Negative_regulation (loss) of Cx3cr1GFP in Monocyte
11) Confidence 0.19 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2965160 Disease Relevance 0.31 Pain Relevance 0.03
In transgenic mice lacking CX3CR1, microglia migrate
Negative_regulation (lacking) of CX3CR1 in microglia associated with targeted disruption
12) Confidence 0.12 Published 2008 Journal PPAR Research Section Body Doc Link PMC2276614 Disease Relevance 1.31 Pain Relevance 0.14

General Comments

This test has worked.

Personal tools
Namespaces

Variants
Actions
Navigation
Toolbox