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etoh, hkac, mddcs, histone, pubmed, alcohol, article, control, panel, google, scholar, cells, chronic, treated, cas, treatment, compared, untreated, cell, acetylation, central, mcp, modifications, human, shows, figure, epigenetic, gene, significantly, modification, effects, supplementary, analysis, exposure, significant, research, fig, shown, increased, carried, nature, role, mass, single, increase, levels, due, stress, chronically, previously,

Topics {✒️}

nature portfolio /nsmb/journal/v18/n1/abs/nsmb privacy policy uv-vis scanning uv-3100pc maldi-ft-icr ms spectra nature genetics 40 nature reviews advertising maldi-ft-icr ms maldi-ft-icr-ms nature maldi matrix peaks reprints primary anti-human h4k12ac-polyclonal alcohol-induced h3k9 hyper-acetylation cell culture media chca matrix peaks supplementary table t1 includes supplementary table t2 displays rabbit anti-human-h4k12ac antibody oxygen-glucose deprivation injury49 hypoxia inducible factor nih/nigms r25 gm061347 post-traumatic stress disorder nuclear regulatory factor-kβ author information authors monocyte-derived dendritic cells ethanol-induced place conditioning imaging flow cytometry elevated mitochondrial superoxide detect post-translational modifications h3 post-translational modifications transcription factor nf-kappab supplementary figure s6 panels show tip60/hat inhibitor arsenic-induced oxidative stress ethanol-exposed adolescent rats site-specific histone acetylation multiple comparison post-test opposite neuro-immunomodulatory effects permissions current research priorities significant dose-dependent downregulation supplementary figure s6 panel histone-modification antibody quality epiquik quantification technique supplementary figure s1 supplementary figure s2 panel author correspondence original author

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• Histone H3 Lys 4 methylation: caught in a bind?

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         headline:Novel detection of post-translational modifications in human monocyte-derived dendritic cells after chronic alcohol exposure: Role of inflammation regulator H4K12ac
         description:Previous reports on epigenetic mechanisms involved in alcohol abuse have focus on hepatic and neuronal regions, leaving the immune system and specifically monocyte-derived dendritic cells (MDDCs) understudied. Our lab has previously shown histone deacetylases are modulated in cells derived from alcohol users and after in vitro acute alcohol treatment of human MDDCs. In the current study, we developed a novel screening tool using matrix assisted laser desorption ionization-fourier transform-ion cyclotron resonance mass spectrometry (MALDI-FT-ICR MS) and single cell imaging flow cytometry to detect post-translational modifications (PTMs) in human MDDCs due to chronic alcohol exposure. Our results demonstrate, for the first time, in vitro chronic alcohol exposure of MDDCs modulates H3 and H4 and induces a significant increase in acetylation at H4K12 (H4K12ac). Moreover, the Tip60/HAT inhibitor, NU9056, was able to block EtOH-induced H4K12ac, enhancing the effect of EtOH on IL-15, RANTES, TGF-β1, and TNF-α cytokines while restoring MCP-2 levels, suggesting that H4K12ac may be playing a major role during inflammation and may serve as an inflammation regulator or a cellular stress response mechanism under chronic alcohol conditions.
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      headline:Novel detection of post-translational modifications in human monocyte-derived dendritic cells after chronic alcohol exposure: Role of inflammation regulator H4K12ac
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