INT86559

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Context Info
Confidence 0.41
First Reported 2000
Last Reported 2010
Negated 0
Speculated 0
Reported most in Body
Documents 8
Total Number 8
Disease Relevance 3.54
Pain Relevance 0.99

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 (KITLG) signal transduction (KITLG) extracellular space (KITLG)
extracellular region (KITLG) cell adhesion (KITLG) plasma membrane (KITLG)
Anatomy Link Frequency
Leydig cell 1
neutrophils 1
KITLG (Homo sapiens)
Pain Link Frequency Relevance Heat
chemokine 20 99.04 Very High Very High Very High
Arthritis 13 94.20 High High
cytokine 84 93.92 High High
Inflammation 118 92.52 High High
rheumatoid arthritis 25 87.76 High High
Osteoarthritis 1 78.84 Quite High
Pain 3 78.12 Quite High
Infliximab 2 63.96 Quite High
interstitial cystitis 5 50.00 Quite Low
COX-2 inhibitor 23 33.84 Quite Low
Disease Link Frequency Relevance Heat
Infection 136 99.38 Very High Very High Very High
Apoptosis 125 98.56 Very High Very High Very High
Cancer 115 97.56 Very High Very High Very High
Disease 67 97.20 Very High Very High Very High
Necrosis 4 95.20 Very High Very High Very High
Arthritis 13 94.20 High High
Hyperplasia 5 92.96 High High
Bacterial Meningitis 14 92.72 High High
Breast Cancer 123 92.52 High High
INFLAMMATION 119 92.52 High High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
Recently, Barbash et al140 demonstrated that attenuation of cyclin D1 SCFFbx4 E3 ubiquitin ligase activity occurs frequently in human cancer and may represent a common mechanism of overexpression and deregulation of cyclin D1.
Negative_regulation (attenuation) of SCF associated with cancer
1) Confidence 0.41 Published 2010 Journal Clinical Medicine Insights. Oncology Section Body Doc Link PMC2883240 Disease Relevance 0.71 Pain Relevance 0
RESULTS: Unstimulated cells released low amounts of MCP-1, IL-6 and SCF.
Negative_regulation (amounts) of SCF
2) Confidence 0.34 Published 2006 Journal J. Urol. Section Body Doc Link 16407046 Disease Relevance 0.17 Pain Relevance 0
They also indicate a downregulation of the SCF receptor in IC.


Negative_regulation (downregulation) of SCF receptor
3) Confidence 0.16 Published 2000 Journal J. Urol. Section Body Doc Link 10688040 Disease Relevance 0 Pain Relevance 0
Intratesticular injection of ghrelin has also been shown to decrease the proliferative activity of differentiating immature Leydig cells in the rat, and this response is associated with a decrease in the mRNA levels of SCF, a putative regulator of Leydig cell development [39].
Negative_regulation (decrease) of SCF in Leydig cell
4) Confidence 0.08 Published 2005 Journal Reprod Biol Endocrinol Section Body Doc Link PMC1291400 Disease Relevance 0.16 Pain Relevance 0
The ability of SCF to enhance migration and morphological alteration was abolished by treatment with SC-236.
Negative_regulation (abolished) of SCF
5) Confidence 0.07 Published 2007 Journal Toxicol. Appl. Pharmacol. Section Abstract Doc Link 17320132 Disease Relevance 0.93 Pain Relevance 0.40
Representative data from one time point of infection shows that there was complete inhibition of SDF-1, SCF, TGF-?
Negative_regulation (inhibition) of SCF associated with infection
6) Confidence 0.05 Published 2010 Journal PLoS Pathogens Section Body Doc Link PMC2820536 Disease Relevance 0.84 Pain Relevance 0.45
The reduction in EQ-5D and SF-6D scores would be expected to mirror the gradual increase in burden of disease.


Negative_regulation (reduction) of SF-6D associated with disease
7) Confidence 0.03 Published 2009 Journal Qual Life Res Section Body Doc Link PMC2761817 Disease Relevance 0.41 Pain Relevance 0.14
Hoxb8 neutrophils were differentiated for 5 days and deprived of SCF for 48 hours, as described for the apoptosis assays.
Negative_regulation (deprived) of SCF in neutrophils associated with apoptosis
8) Confidence 0.01 Published 2009 Journal PLoS Pathogens Section Body Doc Link PMC2682662 Disease Relevance 0.31 Pain Relevance 0

General Comments

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