INT226170

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Context Info
Confidence 0.44
First Reported 2007
Last Reported 2008
Negated 0
Speculated 0
Reported most in Body
Documents 5
Total Number 6
Disease Relevance 3.96
Pain Relevance 0.31

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

cytoplasm (Trim63)
Anatomy Link Frequency
muscle 10
nucleus 2
Trim63 (Mus musculus)
Pain Link Frequency Relevance Heat
Inflammation 44 98.56 Very High Very High Very High
cytokine 22 96.00 Very High Very High Very High
Inflammatory mediators 8 5.00 Very Low Very Low Very Low
fibrosis 4 5.00 Very Low Very Low Very Low
Inflammatory marker 4 5.00 Very Low Very Low Very Low
Pain 4 5.00 Very Low Very Low Very Low
anesthesia 2 5.00 Very Low Very Low Very Low
isoflurane 2 5.00 Very Low Very Low Very Low
Disease Link Frequency Relevance Heat
Muscular Atrophy 26 99.80 Very High Very High Very High
INFLAMMATION 56 98.56 Very High Very High Very High
Frailty 114 98.20 Very High Very High Very High
Acidosis 24 97.28 Very High Very High Very High
Necrosis 4 94.08 High High
Cancer 20 93.72 High High
Chronic Renal Failure 112 91.76 High High
Insulin Resistance 36 91.32 High High
Appetite Loss 40 90.16 High High
Hypertrophy 8 89.20 High High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
In particular, enhanced expression of muscle-specific E3 ligases, MAFbx/atrogin-1 and MuRF1, with function in protein ubiquitination have been shown to mediate proteosome-dependent protein degradation in muscle wasting.
Positive_regulation (enhanced) of Gene_expression (expression) of MuRF1 in muscle associated with frailty
1) Confidence 0.44 Published 2008 Journal PLoS ONE Section Body Doc Link PMC2361191 Disease Relevance 0.68 Pain Relevance 0
In particular, enhanced expression of muscle-specific E3 ligases, MAFbx/atrogin-1 and MuRF1, with function in protein ubiquitination have been shown to mediate proteosome-dependent protein degradation in muscle wasting.
Positive_regulation (mediate) of Gene_expression (expression) of MuRF1 in muscle associated with frailty
2) Confidence 0.44 Published 2008 Journal PLoS ONE Section Body Doc Link PMC2361191 Disease Relevance 0.70 Pain Relevance 0
Akt-P also phosphorylates the forkhead (FoxO) transcription factor, preventing it from entering the nucleus to promote expression of atrogin-1, MuRF-1, and other atrogenes, thereby blocking protein degradation.
Positive_regulation (promote) of Gene_expression (expression) of MuRF-1 in nucleus
3) Confidence 0.19 Published 2007 Journal Pediatr Nephrol Section Body Doc Link PMC2259254 Disease Relevance 0.62 Pain Relevance 0.12
B will cause overproduction of MuRF1 and muscle atrophy [37].
Positive_regulation (overproduction) of Gene_expression (overproduction) of MuRF1 in muscle associated with muscular atrophy
4) Confidence 0.13 Published 2007 Journal Pediatr Nephrol Section Body Doc Link PMC2259254 Disease Relevance 0.66 Pain Relevance 0.05
B), to free NF-B to enter the nucleus and promote MuRF-1 expression, and ultimately, muscle protein degradation.
Positive_regulation (promote) of Gene_expression (expression) of MuRF-1 in muscle
5) Confidence 0.13 Published 2007 Journal Pediatr Nephrol Section Body Doc Link PMC2259254 Disease Relevance 0.65 Pain Relevance 0.14
The rise in muscle protein losses is associated with two catalytic processes: first, caspase-3 is activated to break down the complex structure of muscle; second, there is increased expression of the E3 ubiquitin ligases, atrogin-1 and MuRF-1, to degrade the proteins made available by caspase-3 [35–37] (Fig. 2).
Positive_regulation (increased) of Gene_expression (expression) of MuRF-1 in muscle
6) Confidence 0.13 Published 2007 Journal Pediatr Nephrol Section Body Doc Link PMC2259254 Disease Relevance 0.65 Pain Relevance 0

General Comments

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