INT131808

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Context Info
Confidence 0.16
First Reported 2006
Last Reported 2008
Negated 0
Speculated 0
Reported most in Body
Documents 2
Total Number 15
Disease Relevance 13.46
Pain Relevance 4.61

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

nucleoplasm (Apex1) mitochondrion (Apex1) lyase activity (Apex1)
aging (Apex1) endoplasmic reticulum (Apex1) intracellular (Apex1)
Anatomy Link Frequency
immune cells 4
macrophage 2
brain 2
monocyte 1
reticulum 1
Apex1 (Mus musculus)
Pain Link Frequency Relevance Heat
Inflammation 512 100.00 Very High Very High Very High
cytokine 322 100.00 Very High Very High Very High
Inflammatory mediators 210 100.00 Very High Very High Very High
excitatory amino acid 14 100.00 Very High Very High Very High
Glutamate 14 100.00 Very High Very High Very High
aspirin 8 98.28 Very High Very High Very High
Inflammatory stimuli 28 90.64 High High
Inflammatory response 378 87.88 High High
antagonist 28 86.88 High High
chemokine 70 82.24 Quite High
Disease Link Frequency Relevance Heat
INFLAMMATION 1169 100.00 Very High Very High Very High
Leukemia 14 100.00 Very High Very High Very High
Fever 42 99.40 Very High Very High Very High
Sepsis 1386 97.82 Very High Very High Very High
Injury 196 97.32 Very High Very High Very High
Anaemia 14 93.84 High High
Dengue 14 92.32 High High
Disease 196 90.84 High High
Gynecological Disease 14 90.56 High High
Infection 252 88.92 High High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
In addition, HMGB1 can be
           released passively from damaged cells (Ref. 56)
           or cells infected by viruses (e.g. 
Localization (released) of Ref
1) Confidence 0.16 Published 2008 Journal Expert Reviews in Molecular Medicine Section Body Doc Link PMC2586610 Disease Relevance 0.66 Pain Relevance 0.11
In vitro, exogenous HMGB1 appears to accumulate on the macrophage cell surface within
           4–6 h of HMGB1 incubation (Ref. 84), which correlates with the kinetics of HMGB1-induced release of
           pro-inflammatory cytokines (Ref. 85). 
Localization (release) of Ref in macrophage associated with inflammation and cytokine
2) Confidence 0.14 Published 2008 Journal Expert Reviews in Molecular Medicine Section Body Doc Link PMC2586610 Disease Relevance 0.52 Pain Relevance 0.48
LPS and CpG-DNA) stimulate innate immune cells to release
           a wide array of pro-inflammatory mediators, including nitric oxide (Ref. 16), TNF (Ref. 17), IL-1 (Ref. 18), leukaemia
           inhibitory factor (LIF) (Ref. 19), interferon
           (IFN)-? 
Localization (release) of Ref in immune cells associated with leukemia and inflammatory mediators
3) Confidence 0.14 Published 2008 Journal Expert Reviews in Molecular Medicine Section Body Doc Link PMC2586610 Disease Relevance 1.51 Pain Relevance 0.36
LPS and CpG-DNA) stimulate innate immune cells to release
           a wide array of pro-inflammatory mediators, including nitric oxide (Ref. 16), TNF (Ref. 17), IL-1 (Ref. 18), leukaemia
           inhibitory factor (LIF) (Ref. 19), interferon
           (IFN)-? 
Localization (release) of Ref in immune cells associated with leukemia and inflammatory mediators
4) Confidence 0.14 Published 2008 Journal Expert Reviews in Molecular Medicine Section Body Doc Link PMC2586610 Disease Relevance 1.51 Pain Relevance 0.36
Indeed, administration of
         stearoyl LPC significantly attenuated circulating HMGB1 levels (Ref. 47), indicating that stearoyl LPC protects against experimental
         sepsis partly by facilitating elimination of invading pathogens and partly by attenuating
         systemic HMGB1 accumulation (Ref. 130).


Localization (accumulation) of Ref associated with sepsis
5) Confidence 0.13 Published 2008 Journal Expert Reviews in Molecular Medicine Section Body Doc Link PMC2586610 Disease Relevance 0.49 Pain Relevance 0.19
LPS and CpG-DNA) stimulate innate immune cells to release
           a wide array of pro-inflammatory mediators, including nitric oxide (Ref. 16), TNF (Ref. 17), IL-1 (Ref. 18), leukaemia
           inhibitory factor (LIF) (Ref. 19), interferon
           (IFN)-? 
Localization (release) of Ref in immune cells associated with leukemia and inflammatory mediators
6) Confidence 0.12 Published 2008 Journal Expert Reviews in Molecular Medicine Section Body Doc Link PMC2586610 Disease Relevance 1.63 Pain Relevance 0.40
Therefore, like other cytokines, extracellular HMGB1 may have protective
           roles when released at low amounts (Ref. 107).
           
Localization (released) of Ref associated with cytokine
7) Confidence 0.12 Published 2008 Journal Expert Reviews in Molecular Medicine Section Body Doc Link PMC2586610 Disease Relevance 1.32 Pain Relevance 0.25
LPS and CpG-DNA) stimulate innate immune cells to release
           a wide array of pro-inflammatory mediators, including nitric oxide (Ref. 16), TNF (Ref. 17), IL-1 (Ref. 18), leukaemia
           inhibitory factor (LIF) (Ref. 19), interferon
           (IFN)-? 
Localization (release) of Ref in immune cells associated with leukemia and inflammatory mediators
8) Confidence 0.12 Published 2008 Journal Expert Reviews in Molecular Medicine Section Body Doc Link PMC2586610 Disease Relevance 1.50 Pain Relevance 0.36
In the brain, exogenous HMGB1 induces the release of pro-inflammatory cytokines (Ref.
             86) and excitatory amino acids (such as
           glutamate) (Ref. 87), induces fever (Ref. 88), and exacerbates cerebral ischaemic injury
           (Ref. 89). 
Localization (release) of Ref in brain associated with glutamate, inflammation, injury, fever, excitatory amino acid and cytokine
9) Confidence 0.12 Published 2008 Journal Expert Reviews in Molecular Medicine Section Body Doc Link PMC2586610 Disease Relevance 0.70 Pain Relevance 0.49
In the brain, exogenous HMGB1 induces the release of pro-inflammatory cytokines (Ref.
             86) and excitatory amino acids (such as
           glutamate) (Ref. 87), induces fever (Ref. 88), and exacerbates cerebral ischaemic injury
           (Ref. 89). 
Localization (release) of Ref in brain associated with glutamate, inflammation, injury, fever, excitatory amino acid and cytokine
10) Confidence 0.12 Published 2008 Journal Expert Reviews in Molecular Medicine Section Body Doc Link PMC2586610 Disease Relevance 0.79 Pain Relevance 0.49
Lacking a leader signal sequence, HMGB1 cannot be actively secreted
           via the classical secretory pathway from the endoplasmic reticulum through the Golgi
           complex (Ref. 51). 
Localization (secreted) of Ref in reticulum
11) Confidence 0.12 Published 2008 Journal Expert Reviews in Molecular Medicine Section Body Doc Link PMC2586610 Disease Relevance 0.65 Pain Relevance 0.14
Its aqueous extract
           dose-dependently inhibited LPS-induced HMGB1 release in macrophage and monocyte
           cultures, partly by interfering with HMGB1 cytoplasmic translocation (Ref. 134). 
Localization (translocation) of Ref in monocyte
12) Confidence 0.12 Published 2008 Journal Expert Reviews in Molecular Medicine Section Body Doc Link PMC2586610 Disease Relevance 0.62 Pain Relevance 0.10
Danshen contains abundant red pigments (termed tanshinone I, tanshinone
           IIA, and cryptotanshinone) (Fig. 4), which
           effectively attenuated LPS-induced HMGB1 release (Ref. 135). 
Localization (release) of Ref
13) Confidence 0.12 Published 2008 Journal Expert Reviews in Molecular Medicine Section Body Doc Link PMC2586610 Disease Relevance 0.43 Pain Relevance 0.23
Its aqueous extract
           dose-dependently inhibited LPS-induced HMGB1 release in macrophage and monocyte
           cultures, partly by interfering with HMGB1 cytoplasmic translocation (Ref. 134). 
Localization (translocation) of Ref in macrophage
14) Confidence 0.04 Published 2008 Journal Expert Reviews in Molecular Medicine Section Body Doc Link PMC2586610 Disease Relevance 0.62 Pain Relevance 0.10
Our molecular exploration further revealed that aspirin's suppressive action of NF-kappaB was mediated by its ability to inhibit the nuclear translocation of cytosolic thioredoxin and redox factor-1.
Localization (translocation) of redox factor-1 associated with aspirin
15) Confidence 0.02 Published 2006 Journal Mech. Ageing Dev. Section Abstract Doc Link 16310244 Disease Relevance 0.50 Pain Relevance 0.56

General Comments

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