*Deacetylase inhibitors ( HDACs ) reverse CpG methylation by regulating DNMT1*

General Discussion
#42

Frankly I don’t care unless someone can provide links or instructions to get these substances.

#43

B-HYDROXYBUTYRATE, is over the place as Keto BHB
I placed my order.

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#44

Google the name and add supplement

#45

Suppression of oxidative stress by β-hydroxybutyrate, an endogenous histone deacetylase inhibitor.

#46

Going back to an old post

Abstract 1052: Variable expression of 5-alpha reductase 2 in the aging adult prostate is regulated by DNA methylation

http://cancerres.aacrjournals.org/content/75/15_Supplement/1052.short

Induction of inflammation with lipopolysaccharide (LPS) stimulated the TNFR1/NF-κB/IL-6/DNMT1 pathway, leading to hypermethylation of the SRD5A2 promoter and silencing of SRD5A2, while treatment with both LPS and TNF-alpha inhibitor reversed this pathway and reactivated SRD5A2 .

As you can see LPS and TNF-alpha inhibitor reversed this pathway and reactivated SRD5A2
Now Methylprednisolone the same medication that was administrated to Anonymous is a potent LPS and TNF-alpha inhibitor ** we talked about this before.

Lipopolysaccharide (LPS) stimulated the TNFR1/NF-κB/IL-6/DNMT1 pathway, leading to hypermethylation of the SRD5A2 promoter and silencing of SRD5A2

Now: Histone deacetylase inhibitors (HDACi) suppress inducibility of nuclear factor-κB (NF-kB) by tumor necrosis factor-α receptor-1 (TNFR1) downregulation.

http://cancerres.aacrjournals.org/content/66/8_Supplement/322.1

Histone deacetylase inhibitors suppress (IL-6) production by rheumatoid arthritis firoblast-like synoviocytes and macrophages via modulation of mRNA stability rather than blockade of NF-κB signalling

HDACs, has also been shown to reactivate methylation-silenced genes even in the absence of DNMT inhibitors

I don’t know guys what you think, but I think that we are getting close, we maybe can find the solution before the study is released. lol I am sorry for being a little SARCASTIC…

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#47

Remember this topic ?

Androgen receptor (AR) overexpression and sensitivity to hormones reversed by epigenetic therapy that restores Purα to a transcriptional repressor complex (RC) of AR deregulated in hormone refractory prostate cancer (HRPC) | Journal of Clinical Oncology

Well here also was used HDACs

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