INT135773

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Context Info
Confidence 0.53
First Reported 2006
Last Reported 2010
Negated 0
Speculated 0
Reported most in Body
Documents 31
Total Number 31
Disease Relevance 28.31
Pain Relevance 3.32

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

small molecule metabolic process (HMOX1) endoplasmic reticulum (HMOX1) enzyme binding (HMOX1)
transmembrane transport (HMOX1) signal transducer activity (HMOX1) cytosol (HMOX1)
Anatomy Link Frequency
monocytes 4
intestinal epithelium 4
lung 4
immune system 2
mononuclear cells 2
HMOX1 (Homo sapiens)
Pain Link Frequency Relevance Heat
Inflammation 610 99.60 Very High Very High Very High
Inflammatory response 165 98.88 Very High Very High Very High
ischemia 27 98.16 Very High Very High Very High
cytokine 47 96.08 Very High Very High Very High
cva 9 92.52 High High
rheumatoid arthritis 242 90.36 High High
Infliximab 46 74.56 Quite High
cINOD 31 56.32 Quite High
Arthritis 23 54.40 Quite High
Central nervous system 35 51.44 Quite High
Disease Link Frequency Relevance Heat
Disease 1939 100.00 Very High Very High Very High
Inflammatory Bowel Disease 192 99.74 Very High Very High Very High
INFLAMMATION 786 99.60 Very High Very High Very High
Atherosclerosis 12 99.60 Very High Very High Very High
Lung Cancer 15 99.32 Very High Very High Very High
Stress 88 99.28 Very High Very High Very High
Reperfusion Injury 24 98.92 Very High Very High Very High
Renal Disease 23 98.88 Very High Very High Very High
Hyperplasia 7 98.52 Very High Very High Very High
Rheumatic Diseases 92 98.32 Very High Very High Very High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
Our data support the hypothesis that the expression of the enzyme is defective in lung cancer tissue and are in agreement with a recent study [23] showing reduced HO-1 expression (by IHC methods) in the alveolar macrophages of patients with NSCLC, as compared to controls.
Negative_regulation (reduced) of Gene_expression (expression) of HO-1 in lung associated with lung cancer and non-small-cell lung cancer
1) Confidence 0.53 Published 2010 Journal Journal of Nucleic Acids Section Body Doc Link PMC2911612 Disease Relevance 0.64 Pain Relevance 0
On the other hand, a deficiency in HO-1 expression is associated with severe chronic inflammation, as demonstrated by studies conducted in HO-1 knockout mice [22] and observations in a patient with HO-1 deficiency [23].
Negative_regulation (deficiency) of Gene_expression (expression) of HO-1 associated with targeted disruption and inflammation
2) Confidence 0.45 Published 2008 Journal Arthritis Res Ther Section Body Doc Link PMC2374472 Disease Relevance 1.51 Pain Relevance 0.38
Because TLR4 signaling leads to synthesis of TNF, which may be involved in the reduction in HO-1 expression in PBMCs from patients with BD.
Negative_regulation (reduction) of Gene_expression (expression) of HO-1 associated with disease
3) Confidence 0.45 Published 2008 Journal Arthritis Res Ther Section Body Doc Link PMC2374472 Disease Relevance 0.32 Pain Relevance 0.04
Indeed, HO-1 expression was suppressed in PBMCs stimulated with LPS [29].
Negative_regulation (suppressed) of Gene_expression (expression) of HO-1
4) Confidence 0.45 Published 2008 Journal Arthritis Res Ther Section Body Doc Link PMC2374472 Disease Relevance 1.53 Pain Relevance 0.11
Because LPS (a TLR4 ligand) has been shown to suppress interleukin-10-dependent HO-1 expression in human PBMCs [29], it is plausible that excessively expressed TLR4 contributes to defective HO-1 expression in PBMCs from BD patients.
Negative_regulation (defective) of Gene_expression (expression) of HO-1 associated with disease
5) Confidence 0.45 Published 2008 Journal Arthritis Res Ther Section Body Doc Link PMC2374472 Disease Relevance 0.67 Pain Relevance 0.04
No particular clinical manifestations, including ocular lesions (Table 2) and treatments (data not shown), were associated with the reduction in HO-1 mRNA expression in PBMCs.
Negative_regulation (reduction) of Gene_expression (expression) of HO-1 mRNA
6) Confidence 0.45 Published 2008 Journal Arthritis Res Ther Section Body Doc Link PMC2374472 Disease Relevance 0.78 Pain Relevance 0
Abnormal expression of TLR4 can predispose to defective HO-1 expression in BD PBMCs, because TLR4 may be a putative HO-1 repressor in hepatic ischemia/reperfusion injury mouse model [35].
Negative_regulation (defective) of Gene_expression (expression) of HO-1 associated with reperfusion injury, ischemia and disease
7) Confidence 0.45 Published 2008 Journal Arthritis Res Ther Section Body Doc Link PMC2374472 Disease Relevance 1.49 Pain Relevance 0.13
The data suggest that activation signals through essentially over-expressed TLR4 cause reduction in HO-1 expression in peripheral blood mononuclear cells (PBMC), resulting in an augmentation of inflammatory responses in BD.


Negative_regulation (reduction) of Gene_expression (expression) of HO-1 in mononuclear cells associated with inflammatory response and disease
8) Confidence 0.45 Published 2008 Journal Arthritis Res Ther Section Body Doc Link PMC2374472 Disease Relevance 1.58 Pain Relevance 0.42
Thus, defective expression of HO-1 may be involved in the inflammation characteristic of BD, especially in patients with active disease.
Negative_regulation (defective) of Gene_expression (expression) of HO-1 associated with inflammation and disease
9) Confidence 0.45 Published 2008 Journal Arthritis Res Ther Section Body Doc Link PMC2374472 Disease Relevance 1.25 Pain Relevance 0.23
In our previous study [26] we demonstrated that TNF enhances HO-1 mRNA degradation, resulting in a reduction in HO-1 expression in human monocytes.
Negative_regulation (reduction) of Gene_expression (expression) of HO-1 in monocytes
10) Confidence 0.45 Published 2008 Journal Arthritis Res Ther Section Body Doc Link PMC2374472 Disease Relevance 0.36 Pain Relevance 0.03
In our previous study [26] we showed that TNF suppresses HO-1 expression levels in human peripheral monocytes, thereby accelerating inflammatory responses; this suggests that excessive TNF levels contribute to defective HO-1 expression.
Negative_regulation (defective) of Gene_expression (expression) of HO-1 in monocytes associated with inflammatory response
11) Confidence 0.45 Published 2008 Journal Arthritis Res Ther Section Body Doc Link PMC2374472 Disease Relevance 1.08 Pain Relevance 0.12
Evidence suggests that increased expression of HO-1 can benefit the host in a variety of pathologic conditions, including inflammatory changes, whereas a deficiency in HO-1 expression is associated with vigorous inflammation, as demonstrated by studies of HO-1 knockout mice and observed in a patient with HO-1 deficiency [22,23].
Negative_regulation (deficiency) of Gene_expression (expression) of HO-1 associated with targeted disruption and inflammation
12) Confidence 0.45 Published 2008 Journal Arthritis Res Ther Section Body Doc Link PMC2374472 Disease Relevance 0.97 Pain Relevance 0.22
This effect was abrogated in the presence of the heme oxygenase-1 (HO-1) inhibitor ZnBG.
Negative_regulation (abrogated) of Gene_expression (presence) of HO-1
13) Confidence 0.43 Published 2006 Journal Biochem. Biophys. Res. Commun. Section Abstract Doc Link 16712795 Disease Relevance 0.19 Pain Relevance 0.06
This effect was abrogated in the presence of the heme oxygenase-1 (HO-1) inhibitor ZnBG.
Negative_regulation (abrogated) of Gene_expression (presence) of heme oxygenase-1
14) Confidence 0.43 Published 2006 Journal Biochem. Biophys. Res. Commun. Section Abstract Doc Link 16712795 Disease Relevance 0.19 Pain Relevance 0.06
Overexpression of HO-1 in arterial walls reduces lesion formation as well as intimal hyperplasia subsequent to vascular injury, supporting its vasoprotective function [17-19].
Negative_regulation (reduces) of Gene_expression (Overexpression) of HO-1 associated with vasculitis and hyperplasia
15) Confidence 0.42 Published 2010 Journal J Biomed Sci Section Body Doc Link PMC2841098 Disease Relevance 1.65 Pain Relevance 0.18
Reduced HO-1 mRNA expression in PBMCs from patients with active BD
Negative_regulation (Reduced) of Gene_expression (expression) of HO-1 mRNA associated with disease
16) Confidence 0.40 Published 2008 Journal Arthritis Res Ther Section Body Doc Link PMC2374472 Disease Relevance 0.43 Pain Relevance 0
Moreover, HO-1 expression in PBMCs from patients with Beh├žet's disease was repressed in the presence of either lipopolysaccharide or heat shock protein-60.


Negative_regulation (repressed) of Gene_expression (expression) of HO-1 associated with shock and disease
17) Confidence 0.33 Published 2008 Journal Arthritis Res Ther Section Abstract Doc Link PMC2374472 Disease Relevance 0.88 Pain Relevance 0.07
l; P = 0.77, by Mann-Whitney U-test), indicating that HO-1 expression was reduced in individual cells from patients with active disease.
Negative_regulation (reduced) of Gene_expression (expression) of HO-1 associated with disease
18) Confidence 0.33 Published 2008 Journal Arthritis Res Ther Section Body Doc Link PMC2374472 Disease Relevance 0.79 Pain Relevance 0
In the present study we found endogenous HO-1 expression to be decreased in PBMCs from patients with active BD.
Negative_regulation (decreased) of Gene_expression (expression) of HO-1 associated with disease
19) Confidence 0.33 Published 2008 Journal Arthritis Res Ther Section Body Doc Link PMC2374472 Disease Relevance 0.70 Pain Relevance 0.10
Taken together, our findings suggest that highly expressed TLR4 might contribute to reduced HO-1 expression, leading to an activation of the innate immune system in BD, although other factors including TNF may be involved in the defective HO-1.
Negative_regulation (reduced) of Gene_expression (expression) of HO-1 in immune system associated with disease
20) Confidence 0.33 Published 2008 Journal Arthritis Res Ther Section Body Doc Link PMC2374472 Disease Relevance 0.92 Pain Relevance 0.10

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