INT272886

From wiki-pain
Jump to: navigation, search
Context Info
Confidence 0.23
First Reported 2007
Last Reported 2010
Negated 0
Speculated 0
Reported most in Body
Documents 4
Total Number 6
Disease Relevance 4.63
Pain Relevance 0.69

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

nucleus (Hdac2) enzyme binding (Hdac2) transcription factor binding (Hdac2)
cytoplasm (Hdac2)
Anatomy Link Frequency
epithelial cells 3
macrophages 1
Hdac2 (Mus musculus)
Pain Link Frequency Relevance Heat
Inflammation 465 97.24 Very High Very High Very High
corticosteroid 15 94.76 High High
dexamethasone 6 88.04 High High
Inflammatory response 87 73.48 Quite High
cytokine 78 47.76 Quite Low
chemokine 66 35.52 Quite Low
antagonist 57 34.72 Quite Low
metalloproteinase 60 5.00 Very Low Very Low Very Low
Bioavailability 33 5.00 Very Low Very Low Very Low
Infliximab 15 5.00 Very Low Very Low Very Low
Disease Link Frequency Relevance Heat
Stress 114 99.36 Very High Very High Very High
Chronic Obstructive Pulmonary Disease 324 99.08 Very High Very High Very High
Pulmonary Disease 435 99.04 Very High Very High Very High
Disease 138 98.12 Very High Very High Very High
Repression 6 97.56 Very High Very High Very High
INFLAMMATION 564 97.24 Very High Very High Very High
Nicotine Addiction 177 93.20 High High
Asthma 69 58.88 Quite High
Emphysema 75 5.00 Very Low Very Low Very Low
Apoptosis 45 5.00 Very Low Very Low Very Low

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
Moreover, protein expression of HDAC2 was decreased in a similar manner in COPD patients.
Negative_regulation (decreased) of Gene_expression (expression) of HDAC2 associated with pulmonary disease
1) Confidence 0.23 Published 2007 Journal International Journal of Chronic Obstructive Pulmonary Disease Section Body Doc Link PMC2695202 Disease Relevance 1.06 Pain Relevance 0.18
Thus, the cigarette smoke/oxidant-mediated reduction in HDAC2 levels in alveolar epithelial cells and macrophages will not only increase inflammatory gene expression but will also cause a decrease in glucocorticoid function in patients with COPD.
Negative_regulation (reduction) of Gene_expression (levels) of HDAC2 in epithelial cells associated with pulmonary disease and inflammation
2) Confidence 0.17 Published 2007 Journal International Journal of Chronic Obstructive Pulmonary Disease Section Body Doc Link PMC2695202 Disease Relevance 1.01 Pain Relevance 0.21
Similarly, in models where HDAC-2 activity is compromised, GC function is reduced, and restoration or protection of HDAC-2 activity is correlated with a restoration in GC sensitivity.55,87 Therefore, there is strong evidence that the reduction in HDAC-2 activity and expression seen in patients with COPD is likely to be an important factor in the mechanisms of the relative GC insensitivity in this disease.
Negative_regulation (reduction) of Gene_expression (expression) of HDAC-2 associated with chronic obstructive pulmonary disease and disease
3) Confidence 0.15 Published 2010 Journal International Journal of Chronic Obstructive Pulmonary Disease Section Body Doc Link PMC2939685 Disease Relevance 0.58 Pain Relevance 0.04
Acutely, oxidative stress reduces HDAC-2 activity with a reduction in HDAC-2 protein expression seen with more chronic oxidant exposures in in vitro and in vivo models.71,78,79 This reduction in HDAC-2 activity and expression is strongly associated with oxidant-mediated covalent modifications, including hyperphosphorylation, nitration, and carbonylation, which impair protein activity and enhance proteasomal degradation.72,73,78–83 These modifications are mediated by reactive oxygen, including reactive carbonyls and reactive nitrogen species, and by kinase signaling pathways activated by oxidant stress.72,73,83 Although the exact mechanisms and pathways that regulate these modifications remain unclear, recent work has suggested that oxidants modulate HDAC-2 phosphorylation and subsequent ubiquitination followed by proteasomal degradation through a protein kinase CK2?
Negative_regulation (reduction) of Gene_expression (expression) of HDAC-2 associated with stress
4) Confidence 0.15 Published 2010 Journal International Journal of Chronic Obstructive Pulmonary Disease Section Body Doc Link PMC2939685 Disease Relevance 0.51 Pain Relevance 0.03
Acutely, oxidative stress reduces HDAC-2 activity with a reduction in HDAC-2 protein expression seen with more chronic oxidant exposures in in vitro and in vivo models.71,78,79 This reduction in HDAC-2 activity and expression is strongly associated with oxidant-mediated covalent modifications, including hyperphosphorylation, nitration, and carbonylation, which impair protein activity and enhance proteasomal degradation.72,73,78–83 These modifications are mediated by reactive oxygen, including reactive carbonyls and reactive nitrogen species, and by kinase signaling pathways activated by oxidant stress.72,73,83 Although the exact mechanisms and pathways that regulate these modifications remain unclear, recent work has suggested that oxidants modulate HDAC-2 phosphorylation and subsequent ubiquitination followed by proteasomal degradation through a protein kinase CK2?
Negative_regulation (reduction) of Gene_expression (expression) of HDAC-2 associated with stress
5) Confidence 0.11 Published 2010 Journal International Journal of Chronic Obstructive Pulmonary Disease Section Body Doc Link PMC2939685 Disease Relevance 0.44 Pain Relevance 0.03
Thus, the cigarette smoke/oxidant-mediated reduction in HDAC2 levels in alveolar epithelial cells and macrophages will not only increase inflammatory gene expression but will also cause a decrease in glucocorticoid function in patients with COPD.
Negative_regulation (reduction) of in macrophages Gene_expression (levels) of HDAC2 in epithelial cells associated with pulmonary disease and inflammation
6) Confidence 0.06 Published 2007 Journal International Journal of Chronic Obstructive Pulmonary Disease Section Body Doc Link PMC2695202 Disease Relevance 1.01 Pain Relevance 0.21

General Comments

This test has worked.

Personal tools
Namespaces

Variants
Actions
Navigation
Toolbox