INT278808

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Context Info
Confidence 0.01
First Reported 2009
Last Reported 2009
Negated 0
Speculated 2
Reported most in Body
Documents 1
Total Number 2
Disease Relevance 0
Pain Relevance 0

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

cytosol (POU5F1) nucleoplasm (POU5F1) nucleus (POU5F1)
DNA binding (POU5F1) transcription factor binding (POU5F1) cytoplasm (POU5F1)
Anatomy Link Frequency
myeloid cell 2
POU5F1 (Homo sapiens)
Pain Link Frequency Relevance Heat
cINOD 6 5.00 Very Low Very Low Very Low
aspirin 4 5.00 Very Low Very Low Very Low
cytokine 4 5.00 Very Low Very Low Very Low
Disease Link Frequency Relevance Heat
Leukemia 16 7.88 Low Low
Cancer 14 5.00 Very Low Very Low Very Low
Myeloid Leukemia 12 5.00 Very Low Very Low Very Low
Cytomegalovirus Infection 6 5.00 Very Low Very Low Very Low
Lymphatic System Cancer 4 5.00 Very Low Very Low Very Low
Hematologic Neoplasms 4 5.00 Very Low Very Low Very Low
Chronic Lymphoid Leukemia 4 5.00 Very Low Very Low Very Low
Repression 2 5.00 Very Low Very Low Very Low
Adhesions 2 5.00 Very Low Very Low Very Low
INFLAMMATION 2 5.00 Very Low Very Low Very Low

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
To determine whether this transactivation is dependent on homeodomain-DNA binding, the N51S mutation was introduced into the homeodomain of NUP98-HOXA9 (Fig. 2A).
Spec (whether) Regulation (dependent) of homeodomain-DNA Binding (binding) of
1) Confidence 0.01 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2725295 Disease Relevance 0 Pain Relevance 0
To determine the role of homeodomain-DNA binding in the regulation of transcription by NUP98-HOXA9, luciferase reporter assays were carried out using the K562 human myeloid cell line.
Spec (determine) Regulation (role) of homeodomain-DNA Binding (binding) of in myeloid cell
2) Confidence 0.01 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2725295 Disease Relevance 0 Pain Relevance 0

General Comments

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