INT158374
From wiki-pain
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Sentences Mentioned In
Key: | Protein | Mutation | Event | Anatomy | Negation | Speculation | Pain term | Disease term |
Trichostatin A, a histone deacetylase inhibitor, reduces lesion growth and hyperalgesia in experimentally induced endometriosis in mice. | |||||||||||||||
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VPA is a histone deacetylase inhibitor, and it is possible that the differential teratogenesis in B6 and D2 is because of strain differences in histone acetylation. | |||||||||||||||
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Oral administration of sodium butyrate--a histone deacetylase inhibitor--resulted in the improvement of neurological dysfunction in the SBMA mouse model, although its therapeutic dose range is narrow. | |||||||||||||||
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Although it is very possible that our behavioral phenotypes are a result of the loss of the putative deacetylase domain, they could also be due to the low expression of the N-terminal domain. | |||||||||||||||
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Epigenetic modulation of mGlu2 receptors by histone deacetylase inhibitors in the treatment of inflammatory pain. | |||||||||||||||
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The butyrate moiety of arginine butyrate has been shown to inhibit histone deacetylase, resulting in hyperacetylation of histones H3 and H4. | |||||||||||||||
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It has been reported that the second generation of HPCs (suberoylanilide hydroxamic acid [SAHA]), structurally related to but 2000-fold more potent than HMBA, was an inhibitor of histone deacetylase activity and caused accumulation of hyperacetylated histone H4 in murine erythroleukemia.
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We therefore suggest that the dose and time regimen for histone deacetylase inhibitors, such as SAHA, may have to consider the p53 status of breast cancers.
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SAHA was reported to be a histone deacetylase inhibitor and caused accumulation of hyperacetylated histone H4 in murine erythroleukemia [17]. | |||||||||||||||
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Tumor-deacetylase activity decreased in eight patients in a statistically significant manner. | |||||||||||||||
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Riggs and colleagues identified the HDACs inhibitor prototype sodium butyrate to be an effective inhibitor of deacetylase activity [32, 33]. | |||||||||||||||
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The histone acetyltranferase CREB binding protein CBP is required for recognition memory (Barrett and Wood, 2008 for a review) and histone deacetylase inhibition enhances long-term recognition memory (Stefanko et al., 2009). | |||||||||||||||
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To examine the effects of a histone deacetylase inhibitor, Trichostatin A (TSA), on the behavior of macrophages and subconjunctival fibroblasts in vitro and on ocular surface inflammation and scarring in vivo using an alkali burn wound healing model.
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