INT191925

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Context Info
Confidence 0.68
First Reported 2006
Last Reported 2010
Negated 0
Speculated 0
Reported most in Body
Documents 18
Total Number 18
Disease Relevance 26.99
Pain Relevance 0.83

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

nucleus (Hspb8) intracellular (Hspb8) response to stress (Hspb8)
cytoplasm (Hspb8)
Anatomy Link Frequency
cardiomyocyte 6
apoptotic cell 4
sputum 2
submandibular lymph node 2
Hspb8 (Mus musculus)
Pain Link Frequency Relevance Heat
Inflammation 67 99.88 Very High Very High Very High
Inflammatory marker 2 98.32 Very High Very High Very High
fibrosis 75 95.44 Very High Very High Very High
Central nervous system 15 95.32 Very High Very High Very High
cytokine 18 86.24 High High
tolerance 5 83.20 Quite High
anesthesia 16 33.28 Quite Low
Nicotine 3 5.00 Very Low Very Low Very Low
Neuropeptide 2 5.00 Very Low Very Low Very Low
Inflammatory mediators 2 5.00 Very Low Very Low Very Low
Disease Link Frequency Relevance Heat
Nicotine Addiction 140 99.98 Very High Very High Very High
Pneumonia 11 99.88 Very High Very High Very High
Targeted Disruption 1440 99.80 Very High Very High Very High
Apoptosis 75 99.64 Very High Very High Very High
Death 180 99.58 Very High Very High Very High
Hypersensitivity 74 99.42 Very High Very High Very High
Asthma 265 99.20 Very High Very High Very High
Alzheimer's Dementia 480 99.08 Very High Very High Very High
Coronary Heart Disease 450 98.86 Very High Very High Very High
INFLAMMATION 60 98.32 Very High Very High Very High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
The exact mechanism(s) by which GGA treatment increases HSPB8 expression in HSPB5 R120G TG mice has not been fully elucidated.
Positive_regulation (increases) of Gene_expression (expression) of HSPB8 associated with targeted disruption
1) Confidence 0.68 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2670514 Disease Relevance 1.52 Pain Relevance 0.05
To clarify the functional role of HSPB8 induction on the development of HSPB5 R120G cardiomyopathy and test sufficiency, we generated a TG mouse, in which HSPB8 is overexpressed in a cardiac-specific manner using the inducible ?
Positive_regulation (overexpressed) of Gene_expression (overexpressed) of HSPB8 associated with targeted disruption and coronary heart disease
2) Confidence 0.68 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2670514 Disease Relevance 1.48 Pain Relevance 0.03
In the model tested here, we found that long-term treatment with GGA results in HSPB8 induction and a similar level of overexpression of HSPB8 via transgenic manipulation recapitulates the protective effect of GGA in HSPB5 R120G cardiomyopathy.
Positive_regulation (overexpression) of Gene_expression (overexpression) of HSPB8 associated with targeted disruption and coronary heart disease
3) Confidence 0.68 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2670514 Disease Relevance 0.99 Pain Relevance 0
In the present study, we show that geranylgeranylacetone (GGA), a nontoxic antiulcer drug and inducer of small HSPs [16], can induce expression of HSPB8 and HSPB1 and reduce the formation of amyloid oligomers as well as insoluble aggregates in HSPB5 R120G TG mice.
Positive_regulation (induce) of Gene_expression (expression) of HSPB8 associated with targeted disruption and alzheimer's dementia
4) Confidence 0.68 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2670514 Disease Relevance 1.43 Pain Relevance 0.04
We hypothesized that GGA treatment and overexpression of HSPB8 mediate their effects through reduction in cell death.
Positive_regulation (overexpression) of Gene_expression (overexpression) of HSPB8 associated with death
5) Confidence 0.45 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2670514 Disease Relevance 1.86 Pain Relevance 0.03
These results suggest that GGA treatment and overexpression of HSPB8 inhibit apoptotic cell death through mitochondrial and caspase pathways.


Positive_regulation (overexpression) of Gene_expression (overexpression) of HSPB8 in apoptotic cell associated with apoptosis and death
6) Confidence 0.45 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2670514 Disease Relevance 1.69 Pain Relevance 0
Both GGA treatment and overexpression of HSPB8 resulted in inhibition of cytochrome c release from mitochondria, decreased activation of caspase-3 and attenuated TUNEL-positive cardiomyocyte death in R120G TG mice (Figure 8A–D).
Positive_regulation (overexpression) of Gene_expression (overexpression) of HSPB8 in cardiomyocyte associated with targeted disruption and death
7) Confidence 0.45 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2670514 Disease Relevance 1.83 Pain Relevance 0
Inhibition of apoptotic cell death by GGA treatment or overexpression of HSPB8
Positive_regulation (overexpression) of Gene_expression (overexpression) of HSPB8 in apoptotic cell associated with apoptosis and death
8) Confidence 0.45 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2670514 Disease Relevance 2.03 Pain Relevance 0.03
No significant differences in cardiac function, heart weight, histology or survival rate could be detected in these mice, suggesting that twice the level of overexpression of HSPB8 is nontoxic for cardiomyocytes (Figure 5A–G, Table 1).
Positive_regulation (overexpression) of Gene_expression (overexpression) of HSPB8 in cardiomyocytes
9) Confidence 0.45 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2670514 Disease Relevance 1.56 Pain Relevance 0
Next, we crossbred HSPB8 TG mice with R120G TG mice and generated tTA/HSPB8/R120G triple TG mice, which overexpress HSPB5 R120G and HSPB8 proteins in a cardiac-specific manner.
Positive_regulation (overexpress) of Gene_expression (overexpress) of HSPB8 associated with targeted disruption
10) Confidence 0.45 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2670514 Disease Relevance 1.79 Pain Relevance 0.03
While GGA increased the expression levels of HSPB8 and HSPB1 as well as HSP70 in a dose-dependent manner, no induction of HSPB5 was observed (Figure 1A and B).
Positive_regulation (increased) of Gene_expression (levels) of HSPB8
11) Confidence 0.45 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2670514 Disease Relevance 0.43 Pain Relevance 0
Overexpression of HSPB8 led to a reduction in amyloid oligomer and aggregate formation, resulting in improved cardiac function and survival.
Positive_regulation (Overexpression) of Gene_expression (Overexpression) of HSPB8 associated with alzheimer's dementia
12) Confidence 0.45 Published 2009 Journal PLoS ONE Section Abstract Doc Link PMC2670514 Disease Relevance 1.09 Pain Relevance 0.05
These results imply that the overexpression of HSPB8 is critical to suppress the progression of cardiac disease in HSPB5 R120G TG mice.


Positive_regulation (overexpression) of Gene_expression (overexpression) of HSPB8 associated with targeted disruption and heart disease
13) Confidence 0.45 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2670514 Disease Relevance 2.09 Pain Relevance 0.03
Premature death was completely suppressed by the overexpression of HSPB8 in R120G TG mice (Figure 5G).
Positive_regulation (overexpression) of Gene_expression (overexpression) of HSPB8 associated with targeted disruption and death
14) Confidence 0.45 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2670514 Disease Relevance 1.85 Pain Relevance 0.05
Treatment with GGA as well as the overexpression of HSPB8 also inhibited cytochrome c release from mitochondria, activation of caspase-3 and TUNEL-positive cardiomyocyte death in the R120G TG mice.


Positive_regulation (overexpression) of Gene_expression (overexpression) of HSPB8 in cardiomyocyte associated with death
15) Confidence 0.45 Published 2009 Journal PLoS ONE Section Abstract Doc Link PMC2670514 Disease Relevance 0.92 Pain Relevance 0.04
Cigarette smoking enhances the production of IgE antibodies, stimulates the production of inflammatory markers in the sputum, and causes hyperinflation in older asthmatics (Mitsunobu et al. 2004).
Positive_regulation (enhances) of Gene_expression (production) of IgE in sputum associated with nicotine addiction, inflammatory marker and occupational lung diseases
16) Confidence 0.01 Published 2006 Journal Environ Health Perspect Section Body Doc Link PMC1440793 Disease Relevance 1.97 Pain Relevance 0.05
However, in a BALB/c model examining the development of allergic inflammation, Moerloose et al [93] demonstrated that acute concurrent exposure to allergen (OVA) and MS enhances the allergic pulmonary inflammation, and augments OVA-specific IgE production and airway hyperresponsiveness [93].
Positive_regulation (augments) of Gene_expression (production) of IgE associated with nicotine addiction, inflammation, hypersensitivity and pneumonia
17) Confidence 0.01 Published 2010 Journal Respir Res Section Body Doc Link PMC2831838 Disease Relevance 2.13 Pain Relevance 0.33
In our present model using NC/Nga mice, mite allergen treatment significantly elevated the production of total IgE and allergen-specific IgG1 in serum, increased the number of submandibular lymph node cells, and enhanced cell proliferation of submandibular lymph node cells in the presence of allergen stimulation ex vivo (data not shown).
Positive_regulation (elevated) of Gene_expression (production) of IgE in submandibular lymph node
18) Confidence 0.00 Published 2008 Journal Environ Health Perspect Section Body Doc Link PMC2535612 Disease Relevance 0.34 Pain Relevance 0.07

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