INT236584

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Context Info
Confidence 0.33
First Reported 2008
Last Reported 2010
Negated 0
Speculated 0
Reported most in Body
Documents 2
Total Number 2
Disease Relevance 1.82
Pain Relevance 0.20

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 (Ncoa1) nucleus (Ncoa1) transferase activity, transferring acyl groups (Ncoa1)
DNA binding (Ncoa1) signal transducer activity (Ncoa1)
Ncoa1 (Mus musculus)
Pain Link Frequency Relevance Heat
tolerance 18 80.52 Quite High
agonist 12 79.12 Quite High
Pain 1 63.96 Quite High
anesthesia 3 5.00 Very Low Very Low Very Low
isoflurane 3 5.00 Very Low Very Low Very Low
member 8 2 5.00 Very Low Very Low Very Low
monoamine 2 5.00 Very Low Very Low Very Low
Eae 2 5.00 Very Low Very Low Very Low
opioid receptor 2 5.00 Very Low Very Low Very Low
dexamethasone 1 5.00 Very Low Very Low Very Low
Disease Link Frequency Relevance Heat
Hypersensitivity 1 99.26 Very High Very High Very High
Obesity 30 97.96 Very High Very High Very High
Reprotox - General 1 94 97.64 Very High Very High Very High
Impaired Glucose Tolerance 18 95.48 Very High Very High Very High
Insulin Resistance 8 94.52 High High
Metabolic Disorder 9 85.68 High High
Disease 8 79.16 Quite High
Recurrence 4 75.24 Quite High
Body Weight 12 66.92 Quite High
Pain 1 63.96 Quite High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
Moreover, our data suggest that the coactivators SRC1 and TIF2 are involved in this interaction.
Regulation (involved) of SRC1
1) Confidence 0.33 Published 2008 Journal PLoS Genetics Section Abstract Doc Link PMC2432036 Disease Relevance 0.73 Pain Relevance 0.11
Mechanisms of progression to CRPC that involve or utilize the androgen signaling pathway include: hypersensitivity due to AR gene amplification [5,6]; changes in AR co-regulators such as nuclear receptor coactivators (NCOA1 and NCOA2) [7,8]; intraprostatic de novo synthesis of androgen[9] or metabolism of AR ligands from residual adrenal androgens[10,11]; AR promiscuity of ligand specificity due to mutations[12]; and ligand-independent activation of AR by growth factors [protein kinase A (PKA), interleukin 6 (IL6), and epidermal growth factor (EGF)][13-15].
Regulation (changes) of NCOA1 associated with hypersensitivity and reprotox - general 1
2) Confidence 0.26 Published 2010 Journal BMC Med Genomics Section Body Doc Link PMC2956710 Disease Relevance 1.10 Pain Relevance 0.09

General Comments

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