INT133648

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Context Info
Confidence 0.60
First Reported 2006
Last Reported 2010
Negated 4
Speculated 3
Reported most in Body
Documents 14
Total Number 17
Disease Relevance 10.01
Pain Relevance 2.18

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

nucleus (HDAC9) transcription factor binding (HDAC9) cytoplasm (HDAC9)
Anatomy Link Frequency
lung 1
HDAC9 (Homo sapiens)
Pain Link Frequency Relevance Heat
Inflammation 115 99.96 Very High Very High Very High
agonist 19 99.56 Very High Very High Very High
IPN 5 98.76 Very High Very High Very High
Osteoarthritis 72 96.72 Very High Very High Very High
rheumatoid arthritis 148 96.56 Very High Very High Very High
Antihyperalgesic 4 95.36 Very High Very High Very High
Spinal cord 39 91.68 High High
Thermal hyperalgesia 14 91.20 High High
Lasting pain 12 87.92 High High
Analgesic 4 86.32 High High
Disease Link Frequency Relevance Heat
INFLAMMATION 129 99.96 Very High Very High Very High
Epilepsy 32 99.92 Very High Very High Very High
Inflammatory Pain 6 98.76 Very High Very High Very High
Convulsion 18 98.44 Very High Very High Very High
Cancer 308 98.16 Very High Very High Very High
Toxicity 110 97.48 Very High Very High Very High
Breast Cancer 37 97.20 Very High Very High Very High
Stomach Cancer 36 97.20 Very High Very High Very High
Prostate Cancer 1 97.12 Very High Very High Very High
Frailty 79 96.72 Very High Very High Very High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
We also demonstrate that this marker of functional HDAC inhibition occurs almost immediately (15 min) after exposure of F9 cells to VPA, whereas no influence on the HDAC protein levels (HDAC 2 and HDAC 3) could be detected even after 24 h of treatment.
Neg (no) Regulation (influence) of HDAC
1) Confidence 0.60 Published 2006 Journal Chem. Res. Toxicol. Section Abstract Doc Link 16485903 Disease Relevance 0.28 Pain Relevance 0.06
We also demonstrate that this marker of functional HDAC inhibition occurs almost immediately (15 min) after exposure of F9 cells to VPA, whereas no influence on the HDAC protein levels (HDAC 2 and HDAC 3) could be detected even after 24 h of treatment.
Neg (no) Regulation (influence) of HDAC
2) Confidence 0.60 Published 2006 Journal Chem. Res. Toxicol. Section Abstract Doc Link 16485903 Disease Relevance 0.28 Pain Relevance 0.06
We also demonstrate that this marker of functional HDAC inhibition occurs almost immediately (15 min) after exposure of F9 cells to VPA, whereas no influence on the HDAC protein levels (HDAC 2 and HDAC 3) could be detected even after 24 h of treatment.
Neg (no) Regulation (influence) of HDAC
3) Confidence 0.60 Published 2006 Journal Chem. Res. Toxicol. Section Abstract Doc Link 16485903 Disease Relevance 0.28 Pain Relevance 0.06
In this proof-of-concept study, we demonstrate that treatment with hydralazine and magnesium valproate exerts its proposed molecular effects of DNA demethylation, HDAC inhibition, and gene reactivation in primary tumors of patients with breast cancer.
Spec (proposed) Regulation (effects) of HDAC associated with cancer and breast cancer
4) Confidence 0.37 Published 2006 Journal PLoS ONE Section Body Doc Link PMC1762324 Disease Relevance 0.58 Pain Relevance 0
This class of HDAC also exhibits upregulation in response to CFA, suggesting that the members in class IIa HDACs are potential targets for attenuation of persistent inflammatory pain.
Regulation (targets) of HDAC associated with ipn
5) Confidence 0.26 Published 2010 Journal Mol Pain Section Body Doc Link PMC2942827 Disease Relevance 0.43 Pain Relevance 0.68
agonist pioglitazone and the HDAC inhibitor valproic acid has been reported to
Regulation (reported) of HDAC associated with agonist
6) Confidence 0.25 Published 2008 Journal PPAR Research Section Body Doc Link PMC2408709 Disease Relevance 0.70 Pain Relevance 0.14
In contrast, HDAC inhibitors have been shown to enhance lung and microglial inflammation, suggesting that HDAC inhibitors might modulate inflammation in a cell type-specific manner.
Spec (might) Regulation (modulate) of HDAC in lung associated with inflammation
7) Confidence 0.22 Published 2010 Journal Arthritis Res Ther Section Body Doc Link PMC2945023 Disease Relevance 0.89 Pain Relevance 0.26
Total nuclear HDAC activity (expressed as micromolar values of the deacetylated HDAC substrate standard per 6 ?
Regulation (values) of HDAC
8) Confidence 0.19 Published 2010 Journal Arthritis Res Ther Section Body Doc Link PMC2945023 Disease Relevance 0.63 Pain Relevance 0.31
Therefore, HDAC-2 reduction is involved both glucocorticoid-resistance and NF-?
Regulation (involved) of HDAC
9) Confidence 0.15 Published 2008 Journal Interdisciplinary Toxicology Section Body Doc Link PMC2993477 Disease Relevance 1.22 Pain Relevance 0.23
It was suggested that HDAC-2 is a key enzyme involved in the suppression of NF-?
Regulation (involved) of HDAC
10) Confidence 0.15 Published 2008 Journal Interdisciplinary Toxicology Section Body Doc Link PMC2993477 Disease Relevance 1.22 Pain Relevance 0.24
Tumor deacetylase activity decreased in eight patients with a statistically significant difference between pre and post-treatment values of HDAC activity (p < 0.0264).
Regulation (values) of HDAC associated with cancer
11) Confidence 0.14 Published 2010 Journal J Hematol Oncol Section Body Doc Link PMC2827364 Disease Relevance 0.88 Pain Relevance 0
The aim of the present study was to investigate the relationships between VPA-induced changes in HDAC and Erk1/2 activities, and cell growth and motility.
Spec (investigate) Regulation (changes) of HDAC
12) Confidence 0.07 Published 2010 Journal BMC Cancer Section Body Doc Link PMC2918577 Disease Relevance 0.19 Pain Relevance 0.03
Thus, the hypothesis that compounds that target selectively one HDAC isoform will reveal a greater clinical benefit combined with a better toxicity profile has yet to be proven.
Regulation (target) of HDAC isoform associated with toxicity
13) Confidence 0.06 Published 2010 Journal Clinical Epigenetics Section Body Doc Link PMC3020651 Disease Relevance 0.38 Pain Relevance 0
These relationships suggest that the level of class I HDAC is a reliable maker of prognosis and a specific target for VPA treatment.
Regulation (target) of HDAC
14) Confidence 0.06 Published 2010 Journal J Exp Clin Cancer Res Section Body Doc Link PMC2994814 Disease Relevance 0.81 Pain Relevance 0.10
Highlighting its HDAC inhibitory property and therefore its potential action on some cancers has made this molecule, already well known, a top candidate in new clinical trials.
Regulation (Highlighting) of HDAC associated with cancer
15) Confidence 0.05 Published 2010 Journal Journal of Biomedicine and Biotechnology Section Body Doc Link PMC2926634 Disease Relevance 0.98 Pain Relevance 0
Moreover, given that the balance of acetylation and deacetylation, under the control of HAT and HDAC, is not restricted to histones [29], it can be hypothesized that VPA, like other HDACi, could modulate molecular activity in addition to transcription.
Regulation (control) of HDAC
16) Confidence 0.04 Published 2010 Journal Journal of Biomedicine and Biotechnology Section Body Doc Link PMC2926634 Disease Relevance 0.19 Pain Relevance 0
HDAC 6, 8, and 10 are not modulated.
Neg (not) Regulation (modulated) of HDAC
17) Confidence 0.03 Published 2010 Journal Journal of Biomedicine and Biotechnology Section Body Doc Link PMC2926634 Disease Relevance 0.09 Pain Relevance 0

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