INT126164

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Context Info
Confidence 0.49
First Reported 2005
Last Reported 2010
Negated 0
Speculated 0
Reported most in Body
Documents 15
Total Number 15
Disease Relevance 3.34
Pain Relevance 0.63

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 (Ctsb) mitochondrion (Ctsb) extracellular space (Ctsb)
extracellular region (Ctsb) lysosome (Ctsb) cytoplasm (Ctsb)
Anatomy Link Frequency
nerve 2
Ctsb (Mus musculus)
Pain Link Frequency Relevance Heat
Nerve growth factor 2 100.00 Very High Very High Very High
metalloproteinase 1 91.76 High High
Dismenorea 6 83.76 Quite High
imagery 109 81.12 Quite High
chemokine 27 48.16 Quite Low
cytokine 90 47.56 Quite Low
Inflammatory response 36 44.20 Quite Low
Inflammation 74 43.04 Quite Low
Arthritis 1 13.76 Low Low
Inflammatory mediators 18 5.00 Very Low Very Low Very Low
Disease Link Frequency Relevance Heat
Glioma 79 99.68 Very High Very High Very High
Rupture 27 97.96 Very High Very High Very High
Infection 81 96.80 Very High Very High Very High
Plasmodium Infection 153 96.40 Very High Very High Very High
Cancer 184 96.04 Very High Very High Very High
Metaplasia 2 88.60 High High
Hyperplasia 8 87.64 High High
Hypoxia 11 83.48 Quite High
Colon Cancer 6 81.68 Quite High
Targeted Disruption 35 78.16 Quite High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
Up-regulated genes include those for nerve growth factor (Ngfa), cathepsin B (Ctsb), transforming growth factor beta induced (Tqfbi) and collagens (Colla1, Colla2).
Positive_regulation (Up-regulated) of cathepsin B in nerve associated with nerve growth factor
1) Confidence 0.49 Published 2005 Journal Exp. Toxicol. Pathol. Section Abstract Doc Link 15816354 Disease Relevance 0.51 Pain Relevance 0.27
Up-regulated genes include those for nerve growth factor (Ngfa), cathepsin B (Ctsb), transforming growth factor beta induced (Tqfbi) and collagens (Colla1, Colla2).
Positive_regulation (Up-regulated) of Ctsb in nerve associated with nerve growth factor
2) Confidence 0.43 Published 2005 Journal Exp. Toxicol. Pathol. Section Abstract Doc Link 15816354 Disease Relevance 0.51 Pain Relevance 0.27
We showed that specific inhibition of Syk blocked the Hz-induced cathepsin B activation.
Positive_regulation (activation) of cathepsin B
3) Confidence 0.12 Published 2009 Journal PLoS Pathogens Section Body Doc Link PMC2722371 Disease Relevance 0 Pain Relevance 0
The idea of transient activation of cathepsin B by Hz is supported by the absence of cathepsin B in the supernatant of cells stimulated with Hz and the absence of lysosomal damage upon Hz treatment.
Positive_regulation (activation) of cathepsin B
4) Confidence 0.12 Published 2009 Journal PLoS Pathogens Section Body Doc Link PMC2722371 Disease Relevance 0 Pain Relevance 0
Finally, Syk was found to control the activation of cathepsin B and Hz-induced IL-1?
Positive_regulation (activation) of cathepsin B
5) Confidence 0.12 Published 2009 Journal PLoS Pathogens Section Body Doc Link PMC2722371 Disease Relevance 0 Pain Relevance 0
The first protease-sensing optical probes were autoquench fluorescent probes that convert from a nonfluorescent to a fluorescent state by proteolytic activation of lysosomal cysteine or serine proteases like cathepsin-B [67].
Positive_regulation (activation) of cathepsin-B
6) Confidence 0.10 Published 2010 Journal Angiogenesis Section Body Doc Link PMC2911541 Disease Relevance 0.49 Pain Relevance 0.09
requires phagocytosis, ROS generation, potassium efflux and cathepsin B activation without phagosome damage
Positive_regulation (activation) of cathepsin B
7) Confidence 0.09 Published 2009 Journal PLoS Pathogens Section Body Doc Link PMC2722371 Disease Relevance 0.79 Pain Relevance 0
Another interesting observation is that Hz-activated cathepsin B occurred in the intracellular compartment and is rapidly quenched (1–3 hours), suggesting either a transient activation or cathepsin B release into the cytosol.
Positive_regulation (activated) of cathepsin B
8) Confidence 0.09 Published 2009 Journal PLoS Pathogens Section Body Doc Link PMC2722371 Disease Relevance 0 Pain Relevance 0
The mechanism utilized by Hz-activated cathepsin B to modulate the inflammasome remains unclear.
Positive_regulation (activated) of cathepsin B
9) Confidence 0.09 Published 2009 Journal PLoS Pathogens Section Body Doc Link PMC2722371 Disease Relevance 0 Pain Relevance 0
production was dependent on cathepsin B activation, similar to other inflammasome activators such as silica, MSU [17] or nigericin [24].
Positive_regulation (activation) of cathepsin B
10) Confidence 0.09 Published 2009 Journal PLoS Pathogens Section Body Doc Link PMC2722371 Disease Relevance 0 Pain Relevance 0
Another possible mechanism is that Syk could be controlling the NLRP3 inflammasome by regulating cathepsin B activation.
Positive_regulation (activation) of cathepsin B
11) Confidence 0.08 Published 2009 Journal PLoS Pathogens Section Body Doc Link PMC2722371 Disease Relevance 0 Pain Relevance 0
production in an inflammasome-dependent manner that required active cathepsin B, we did not find evidence of Hz-induced lysosomal rupture as previously reported with silica [17].
Positive_regulation (required) of cathepsin B associated with rupture
12) Confidence 0.08 Published 2009 Journal PLoS Pathogens Section Body Doc Link PMC2722371 Disease Relevance 0.25 Pain Relevance 0
Since we observed p27Kip1 upregulation with decreased cell proliferation and G0/G1 phase arrest with the depletion of cathepsin B and uPAR, we next determined the expression of FOXO proteins, which are important transcriptional regulators of the p27Kip1 promoter.
Positive_regulation (upregulation) of cathepsin B
13) Confidence 0.06 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2908539 Disease Relevance 0 Pain Relevance 0
Various reports have demonstrated that cathepsin B and uPAR levels are overexpressed during glioma progression [28]–[30].
Positive_regulation (overexpressed) of cathepsin B associated with glioma
14) Confidence 0.06 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2908539 Disease Relevance 0.78 Pain Relevance 0
Expression of p27Kip1 is influenced by the upregulation of FOXO3a proteins in cathepsin B and uPAR depleted cells
Positive_regulation (upregulation) of cathepsin B
15) Confidence 0.06 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2908539 Disease Relevance 0 Pain Relevance 0

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