INT331786

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Context Info
Confidence 0.11
First Reported 2010
Last Reported 2010
Negated 0
Speculated 1
Reported most in Body
Documents 1
Total Number 2
Disease Relevance 1.20
Pain Relevance 0.08

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)
Hdac2 (Mus musculus)
Pain Link Frequency Relevance Heat
Inflammation 110 91.56 High High
Inflammatory response 48 66.52 Quite High
dexamethasone 2 37.84 Quite Low
cINOD 6 5.00 Very Low Very Low Very Low
chemokine 4 5.00 Very Low Very Low Very Low
cytokine 2 5.00 Very Low Very Low Very Low
withdrawal 2 5.00 Very Low Very Low Very Low
Inflammatory marker 2 5.00 Very Low Very Low Very Low
metalloproteinase 2 5.00 Very Low Very Low Very Low
agonist 2 5.00 Very Low Very Low Very Low
Disease Link Frequency Relevance Heat
Stress 30 99.98 Very High Very High Very High
Repression 4 98.80 Very High Very High Very High
Nicotine Addiction 20 94.12 High High
Chronic Obstructive Pulmonary Disease 216 93.24 High High
INFLAMMATION 164 91.56 High High
Asthma 22 60.12 Quite High
Disease 66 44.08 Quite Low
Apoptosis 16 5.00 Very Low Very Low Very Low
Death 10 5.00 Very Low Very Low Very Low
Bronchitis 8 5.00 Very Low Very Low Very Low

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
protects GC function appears to be mediated through the protection of HDAC-2 activity, it is also likely to include modulation of other corepressors, such as Mi-2 and mSin3a.55,97 The mechanism by which PI3K?
Negative_regulation (protection) of HDAC-2 Binding (activity) of
1) Confidence 0.11 Published 2010 Journal International Journal of Chronic Obstructive Pulmonary Disease Section Body Doc Link PMC2939685 Disease Relevance 0.68 Pain Relevance 0.05
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 (reduces) of HDAC-2 Spec (unclear) Binding (activity) of associated with stress
2) Confidence 0.11 Published 2010 Journal International Journal of Chronic Obstructive Pulmonary Disease Section Body Doc Link PMC2939685 Disease Relevance 0.52 Pain Relevance 0.03

General Comments

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