INT114362

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Context Info
Confidence 0.78
First Reported 2003
Last Reported 2010
Negated 0
Speculated 2
Reported most in Body
Documents 127
Total Number 154
Disease Relevance 120.28
Pain Relevance 23.26

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

extracellular space (Hmgb1) extracellular region (Hmgb1) cell morphogenesis (Hmgb1)
nucleolus (Hmgb1) chromosome (Hmgb1) nucleus (Hmgb1)
Anatomy Link Frequency
macrophage 13
liver 12
monocyte 8
nucleus 4
hepatocytes 4
Hmgb1 (Mus musculus)
Pain Link Frequency Relevance Heat
cytokine 2923 100.00 Very High Very High Very High
Inflammation 2561 100.00 Very High Very High Very High
agonist 294 100.00 Very High Very High Very High
ischemia 1913 99.92 Very High Very High Very High
Inflammatory response 1318 99.42 Very High Very High Very High
chemokine 336 99.04 Very High Very High Very High
Eae 6 98.98 Very High Very High Very High
tolerance 66 98.42 Very High Very High Very High
Nicotine 79 98.30 Very High Very High Very High
cva 307 96.40 Very High Very High Very High
Disease Link Frequency Relevance Heat
Cancer 6926 100.00 Very High Very High Very High
INFLAMMATION 4381 100.00 Very High Very High Very High
Necrosis 311 100.00 Very High Very High Very High
Cv Unclassified Under Development 1883 99.92 Very High Very High Very High
Myocardial Infarction 64 99.92 Very High Very High Very High
Glioma 736 99.86 Very High Very High Very High
Apoptosis 703 99.86 Very High Very High Very High
Disease 705 99.84 Very High Very High Very High
Hemorrhagic Shock 287 99.82 Very High Very High Very High
Glioblastoma 960 99.76 Very High Very High Very High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
For instance, it is not known whether EGCG-mediated suppression of HMGB1 release is dependent on its antioxidant activities, because some antioxidants (e.g., catechin, ethyl gallate) failed to inhibit LPS-induced HMGB1 release.
Localization (release) of HMGB1
1) Confidence 0.78 Published 2007 Journal PLoS ONE Section Body Doc Link PMC2048740 Disease Relevance 0.17 Pain Relevance 0.03
In conclusion, we demonstrated a major tea component, EGCG, recapitulated green tea's HMGB1-inhibiting activities, and dose-dependently abrogated LPS-induced HMGB1 release in macrophage/monocyte cultures.
Localization (release) of HMGB1 in monocyte
2) Confidence 0.78 Published 2007 Journal PLoS ONE Section Body Doc Link PMC2048740 Disease Relevance 0.88 Pain Relevance 0.07
Although EGCG-mediated suppression of HMGB1 cell surface clustering may not account for its inhibitory effects on LPS-induced HMGB1 release, it likely underlies its inhibitory effects on cytokine activities of the secreted HMGB1.
Localization (release) of HMGB1 associated with cytokine
3) Confidence 0.78 Published 2007 Journal PLoS ONE Section Body Doc Link PMC2048740 Disease Relevance 0.34 Pain Relevance 0.20
Although EGCG-mediated suppression of HMGB1 cell surface clustering may not account for its inhibitory effects on LPS-induced HMGB1 release, it likely underlies its inhibitory effects on cytokine activities of the secreted HMGB1.
Localization (secreted) of HMGB1 associated with cytokine
4) Confidence 0.78 Published 2007 Journal PLoS ONE Section Body Doc Link PMC2048740 Disease Relevance 0.43 Pain Relevance 0.17
Therefore, agents proven clinically safe, and yet still capable of attenuating HMGB1 release may hold potential in the prevention and treatment of inflammatory diseases.
Localization (release) of HMGB1 associated with inflammation and disease
5) Confidence 0.78 Published 2007 Journal PLoS ONE Section Body Doc Link PMC2048740 Disease Relevance 1.41 Pain Relevance 0.35
Even at concentrations up to 10 µM, catechin or ethyl gallate did not affect LPS-induced HMGB1 release (Fig. 4B), indicating that functional groups of both catechin and gallate are needed for EGCG's HMGB1-inhibiting properties.


Localization (release) of HMGB1
6) Confidence 0.78 Published 2007 Journal PLoS ONE Section Body Doc Link PMC2048740 Disease Relevance 0.16 Pain Relevance 0.03
For instance, it is not known whether EGCG-mediated suppression of HMGB1 release is dependent on its antioxidant activities, because some antioxidants (e.g., catechin, ethyl gallate) failed to inhibit LPS-induced HMGB1 release.
Localization (release) of HMGB1
7) Confidence 0.78 Published 2007 Journal PLoS ONE Section Body Doc Link PMC2048740 Disease Relevance 0.20 Pain Relevance 0.03
In light of the capacity of EGCG in inhibiting LPS-induced HMGB1 release and cytokine activities, we explored its efficacy in animal models of lethal endotoxemia and sepsis (induced by cecal ligation and puncture).
Localization (release) of HMGB1 in puncture associated with endotoxemia, sepsis and cytokine
8) Confidence 0.78 Published 2007 Journal PLoS ONE Section Body Doc Link PMC2048740 Disease Relevance 0.52 Pain Relevance 0.17
In light of the capacity of EGCG in attenuating LPS-induced HMGB1 release, we explored its efficacy in animal model of lethal endotoxemia.
Localization (release) of HMGB1 associated with endotoxemia
9) Confidence 0.78 Published 2007 Journal PLoS ONE Section Body Doc Link PMC2048740 Disease Relevance 0.39 Pain Relevance 0.03
The mechanism underlying EGCG-mediated suppression of HMGB1 release remains elusive.
Localization (release) of HMGB1
10) Confidence 0.78 Published 2007 Journal PLoS ONE Section Body Doc Link PMC2048740 Disease Relevance 0.05 Pain Relevance 0
Similarly, it is not yet known whether EGCG inhibits LPS-induced HMGB1 release through inhibiting LPS-induced cytoplasmic translocation, or post-translational modification (such as acetylation or phosphorylation).
Localization (release) of HMGB1
11) Confidence 0.78 Published 2007 Journal PLoS ONE Section Body Doc Link PMC2048740 Disease Relevance 0.22 Pain Relevance 0.04
Since receptor clustering-disrupting agents (such as nystatin or MCD) can prevent LPS-induced cytokine production [38], it will thus be interesting to determine whether EGCG inhibits HMGB1 release via similar mechanisms.
Localization (release) of HMGB1 associated with cytokine
12) Confidence 0.78 Published 2007 Journal PLoS ONE Section Body Doc Link PMC2048740 Disease Relevance 0.33 Pain Relevance 0.21
It remains possible that HMGB1 protein is released in brain in response to LPS.
Localization (released) of HMGB1 in brain
13) Confidence 0.77 Published 2003 Journal Cytokine Section Abstract Doc Link 14609567 Disease Relevance 0.49 Pain Relevance 0.51
Interestingly, it was recently shown that HMGB1 released from lymphoma, breast, and colon tumor cells enhances tumor regression induced by standard chemotherapeutic agents by activating TLR4 [9].
Localization (released) of HMGB1 in colon associated with lymphatic system cancer, cancer and colon cancer
14) Confidence 0.73 Published 2009 Journal PLoS Medicine Section Body Doc Link PMC2621261 Disease Relevance 0.96 Pain Relevance 0
We next investigated whether HMGB1 was released into the serum of GBM-bearing mice treated with Ad-TK + GCV and Flt3L in vivo.
Localization (released) of HMGB1 in GBM associated with glioblastoma
15) Confidence 0.73 Published 2009 Journal PLoS Medicine Section Body Doc Link PMC2621261 Disease Relevance 0.86 Pain Relevance 0.04
We then performed a HMGB1-specific ELISA to quantitate the levels of HMGB1 release from GL26, LLc1, GL261, or B16-F10 cells in vitro following treatment with either Ad-TK (+GCV), radiation, or temozolomide.
Localization (release) of HMGB1 in B16-F10
16) Confidence 0.73 Published 2009 Journal PLoS Medicine Section Body Doc Link PMC2621261 Disease Relevance 0.67 Pain Relevance 0
2 = 0.75; Figure 7B) indicating that HMGB1 secreted from GL26 cells stimulates TLR2 signaling.
Localization (secreted) of HMGB1
17) Confidence 0.73 Published 2009 Journal PLoS Medicine Section Body Doc Link PMC2621261 Disease Relevance 0.94 Pain Relevance 0.05
Finally, the researchers report that other tumor cell types release HMGB1 when they are killed and that the Flt3L/TK expression strategy can also kill other tumors growing in mouse brains.


Localization (release) of HMGB1 in brains associated with cancer
18) Confidence 0.73 Published 2009 Journal PLoS Medicine Section Abstract Doc Link PMC2621261 Disease Relevance 1.28 Pain Relevance 0
Herein we uncovered a novel pathway for the activation of an effective anti-GBM immune response mediated by high-mobility-group box 1 (HMGB1), an alarmin protein released from dying tumor cells, which acts as an endogenous ligand for Toll-like receptor 2 (TLR2) signaling on bone marrow-derived GBM-infiltrating DCs.


Localization (released) of HMGB1 in bone marrow associated with cancer and glioblastoma
19) Confidence 0.73 Published 2009 Journal PLoS Medicine Section Abstract Doc Link PMC2621261 Disease Relevance 1.15 Pain Relevance 0.05
Our results demonstrate that glioma-derived HMGB1 released from dying cells is necessary for the clonal expansion of CD8+ T cells specific for glioma antigens including the Trp2180–188 peptide (H-2Kb), and that the effects of HMGB1 are mediated through TLR2 signaling on tumor-infiltrating DCs.
Localization (released) of HMGB1 in T cells associated with cancer and glioma
20) Confidence 0.73 Published 2009 Journal PLoS Medicine Section Body Doc Link PMC2621261 Disease Relevance 1.24 Pain Relevance 0.11

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