INT234417

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Context Info
Confidence 0.37
First Reported 2008
Last Reported 2010
Negated 0
Speculated 0
Reported most in Body
Documents 4
Total Number 4
Disease Relevance 3.65
Pain Relevance 0.03

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

cytosol (ABL1) protein modification process (ABL1) mitochondrion (ABL1)
nucleolus (ABL1) nucleus (ABL1) DNA binding (ABL1)
ABL1 (Homo sapiens)
Pain Link Frequency Relevance Heat
antagonist 4 68.80 Quite High
metalloproteinase 2 43.00 Quite Low
cytokine 9 34.52 Quite Low
agonist 11 22.72 Low Low
imagery 2 11.88 Low Low
Inflammation 10 5.00 Very Low Very Low Very Low
chemokine 3 5.00 Very Low Very Low Very Low
Nicotine 2 5.00 Very Low Very Low Very Low
palliative 2 5.00 Very Low Very Low Very Low
cINOD 2 5.00 Very Low Very Low Very Low
Disease Link Frequency Relevance Heat
Familial Dysautonomia 121 96.80 Very High Very High Very High
Myeloid Leukemia 78 92.72 High High
Disease 32 89.88 High High
Cancer 42 89.52 High High
Leukemia 58 88.44 High High
Myelodysplastic Syndromes 80 84.96 Quite High
Apoptosis 103 79.80 Quite High
Chronic Neutrophilic Leukemia 14 74.64 Quite High
Hyperplasia 4 69.44 Quite High
Myeloproliferative Disorder 91 65.04 Quite High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
In addition to BCR-ABL1 gene amplification resulting in overexpression of BCR-ABL1 protein, or point mutations that prevent the binding of the inhibitor to the kinase domain [8, 9], several groups have demonstrated other forms of BCR-ABL1-independent imatinib resistance [10–12].
Positive_regulation (resulting) of Gene_expression (overexpression) of BCR-ABL1
1) Confidence 0.37 Published 2010 Journal Invest New Drugs Section Body Doc Link PMC3003795 Disease Relevance 0.89 Pain Relevance 0
Since gene expression quantification using RT-qPCR requires a steady reference gene, we selected three genes frequently used for normalization of the data, ABL1, RPLP0, and HPRT1.
Positive_regulation (requires) of Gene_expression (expression) of ABL1
2) Confidence 0.31 Published 2010 Journal PLoS ONE Section Body Doc Link PMC3004942 Disease Relevance 0.54 Pain Relevance 0
In addition to BCR-ABL1 gene amplification resulting in overexpression of BCR-ABL1 protein, or point mutations that prevent the binding of the inhibitor to the kinase domain [8, 9], several groups have demonstrated other forms of BCR-ABL1-independent imatinib resistance [10–12].
Positive_regulation (overexpression) of Gene_expression (overexpression) of BCR-ABL1
3) Confidence 0.25 Published 2010 Journal Invest New Drugs Section Body Doc Link PMC3003795 Disease Relevance 0.88 Pain Relevance 0
This translocation generates a fusion protein called BCR-ABL which
Positive_regulation (generates) of Gene_expression (generates) of BCR-ABL
4) Confidence 0.15 Published 2008 Journal PPAR Research Section Body Doc Link PMC2408681 Disease Relevance 1.34 Pain Relevance 0.03

General Comments

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