INT287043

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Context Info
Confidence 0.57
First Reported 2009
Last Reported 2010
Negated 0
Speculated 0
Reported most in Body
Documents 7
Total Number 9
Disease Relevance 2.81
Pain Relevance 0.36

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

nucleus (Irf4) DNA binding (Irf4) cytoplasm (Irf4)
Anatomy Link Frequency
plasma cell 5
A20 3
Irf4 (Mus musculus)
Pain Link Frequency Relevance Heat
Inflammation 48 85.36 High High
cytokine 42 84.28 Quite High
rheumatoid arthritis 15 17.76 Low Low
antagonist 9 5.00 Very Low Very Low Very Low
anesthesia 6 5.00 Very Low Very Low Very Low
corticosteroid 3 5.00 Very Low Very Low Very Low
agonist 3 5.00 Very Low Very Low Very Low
cINOD 3 5.00 Very Low Very Low Very Low
Disease Link Frequency Relevance Heat
Lymphatic System Cancer 72 100.00 Very High Very High Very High
Necrosis 6 99.60 Very High Very High Very High
Systemic Lupus Erythematosus 183 99.44 Very High Very High Very High
Cancer 24 99.24 Very High Very High Very High
Autoimmune Disease 69 96.80 Very High Very High Very High
Epstein-barr Virus 90 91.60 High High
INFLAMMATION 48 85.36 High High
Disease 48 78.76 Quite High
Sarcoma 12 61.20 Quite High
Targeted Disruption 6 60.48 Quite High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
Induction of IRF4 is of significant interest because it has been shown to play critical roles in both isotype switching during the germinal center reaction, and plasma cell differentiation [2],[37].
Positive_regulation (Induction) of IRF4 in plasma cell
1) Confidence 0.57 Published 2009 Journal PLoS Pathogens Section Body Doc Link PMC2777334 Disease Relevance 0.11 Pain Relevance 0
Finally, as we have shown here, M2 also upregulates the expression of IRF4 [we have observed both M2-driven upregulation of IRF4 transcripts (Fig. 6C) and IRF4 protein (data not shown) in BCL-1 cells].
Positive_regulation (upregulation) of IRF4
2) Confidence 0.41 Published 2009 Journal PLoS Pathogens Section Body Doc Link PMC2777334 Disease Relevance 0.06 Pain Relevance 0
Although the signal(s) that initiate plasma cell differentiation remain controversial, recent progress has identified several critical transcriptional regulators of plasma cell differentiation - including B lymphocyte induced maturation protein 1 (Blimp-1), interferon regulatory factor-4 (IRF-4) and XBP-1s [2],[3],[4],[5],[6].
Positive_regulation (induced) of interferon regulatory factor-4 in plasma cell
3) Confidence 0.41 Published 2009 Journal PLoS Pathogens Section Body Doc Link PMC2777334 Disease Relevance 0.36 Pain Relevance 0
Although the signal(s) that initiate plasma cell differentiation remain controversial, recent progress has identified several critical transcriptional regulators of plasma cell differentiation - including B lymphocyte induced maturation protein 1 (Blimp-1), interferon regulatory factor-4 (IRF-4) and XBP-1s [2],[3],[4],[5],[6].
Positive_regulation (induced) of IRF-4 in plasma cell
4) Confidence 0.41 Published 2009 Journal PLoS Pathogens Section Body Doc Link PMC2777334 Disease Relevance 0.36 Pain Relevance 0
Among the genes that were upregulated upon expression of M2 in the BCL-1 B lymphoma cell line was the cellular transcription factor IRF4 (Fig. 6C, and unpublished data), which has been shown to be required for both isotype switching as well as plasma cell differentiation [2].
Positive_regulation (upregulated) of IRF4 in plasma cell associated with lymphatic system cancer
5) Confidence 0.38 Published 2009 Journal PLoS Pathogens Section Body Doc Link PMC2777334 Disease Relevance 0.10 Pain Relevance 0
Compared to M2.Stop transfected cells, there was a significant induction in the levels of transcripts encoding several plasma cell-associated factors (XBP-1s, Blimp-1, J chain and IRF-4); changes that were also observed upon LPS stimulation of the BCL-1 cell line (Fig. 6C).
Positive_regulation (induction) of IRF-4 in plasma cell
6) Confidence 0.38 Published 2009 Journal PLoS Pathogens Section Body Doc Link PMC2777334 Disease Relevance 0.14 Pain Relevance 0
Currently, active research on this topic is concerned with negatively regulating molecules that activate TLR-dependent signaling, but what about activating some of the natural inhibitory proteins, such as Triad3A, MyD88s, SHP-1, IRAK-M, IRAK1c, IRF4, and A20?
Positive_regulation (activate) of IRF4 in A20
7) Confidence 0.30 Published 2010 Journal Mediators of Inflammation Section Body Doc Link PMC2945668 Disease Relevance 0.65 Pain Relevance 0.08
-induced protein 3 (TNFAIP3, or A20) and IRF4.
Positive_regulation (induced) of IRF4 in A20
8) Confidence 0.30 Published 2010 Journal Mediators of Inflammation Section Body Doc Link PMC2945668 Disease Relevance 0.26 Pain Relevance 0.14
Similarly, promoting the production or activity of the other endogenous TLR signaling inhibitors, Triad3A, MyD88s, SHP-1, IRAK1c, IRF4, or A20, could provide additional options for effective treatment for systemic autoimmunity.
Positive_regulation (promoting) of IRF4 in A20 associated with autoimmune disease
9) Confidence 0.28 Published 2010 Journal Mediators of Inflammation Section Body Doc Link PMC2945668 Disease Relevance 0.79 Pain Relevance 0.14

General Comments

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