INT331778

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Context Info
Confidence 0.11
First Reported 2010
Last Reported 2010
Negated 0
Speculated 0
Reported most in Body
Documents 1
Total Number 1
Disease Relevance 0.49
Pain Relevance 0.03

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
Inflammatory response 24 67.36 Quite High
Inflammation 55 5.00 Very Low Very Low Very Low
cINOD 3 5.00 Very Low Very Low Very Low
chemokine 2 5.00 Very Low Very Low Very Low
cytokine 1 5.00 Very Low Very Low Very Low
dexamethasone 1 5.00 Very Low Very Low Very Low
withdrawal 1 5.00 Very Low Very Low Very Low
Inflammatory marker 1 5.00 Very Low Very Low Very Low
metalloproteinase 1 5.00 Very Low Very Low Very Low
agonist 1 5.00 Very Low Very Low Very Low
Disease Link Frequency Relevance Heat
Stress 15 97.14 Very High Very High Very High
Repression 2 69.80 Quite High
INFLAMMATION 82 67.36 Quite High
Disease 33 64.88 Quite High
Chronic Obstructive Pulmonary Disease 108 55.52 Quite High
Asthma 11 31.12 Quite Low
Nicotine Addiction 10 5.00 Very Low Very Low Very Low
Apoptosis 8 5.00 Very Low Very Low Very Low
Death 5 5.00 Very Low Very Low Very Low
Bronchitis 4 5.00 Very Low Very Low Very Low

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
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?
Regulation (modulate) of Phosphorylation (phosphorylation) of HDAC-2 associated with stress
1) Confidence 0.11 Published 2010 Journal International Journal of Chronic Obstructive Pulmonary Disease Section Body Doc Link PMC2939685 Disease Relevance 0.49 Pain Relevance 0.03

General Comments

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