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C) H3K9 acetylation status analyzed by immunoblotting after transfection of HEK293T cells with a no-insert control (NOI), HDAC1, HDAC2, HDAC3, or HDAC4, followed by histone extraction to examine the relative enzymatic effect of these HDACs on this residue; blots were quantified by densitometric analysis and values shown represent three independent experiments.
David Artis PhD, associate professor of Microbiology, and colleagues report that the enzyme HDAC3 is a key mediator in maintaining proper intestinal integrity and function in the presence of friendly bacteria.
In 2011, Wood's group deleted the HDAC3 gene in a small group of hippocampal neurons in mice.
Recent studies also have shown that liver-specific knockout of the gene encoding HDAC3 in mice leads to severe hepatic steatosis and increased expression of lipogenic genes, although whether HDAC3 expression or function is altered by ethanol has yet to be elucidated (Sun et al.
NF-KB/p65 antagonizes Nrf2ARE pathway by depriving CBP from Nrf2 and facilitating recruitment of HDAC3 to MafK.
Wood, which demonstrates that one of Repligen's HDAC3 inhibitors improves both the acquisition and persistence of long-term memory in an animal model.
Human HDAC7 histone deacetylase activity is associated with HDAC3 in vivo.
Cells of high-fat-diet-induced fatty livers in wild-type mice were characterized by larger lipid droplets, but liver-specific HDAC3 knockout mice on a high-fat diet were characterized by smaller lipid droplets, even though the total lipid content increased versus the wild-type mice.
1 Mechanism of Action Vorinostat inhibits the enzymatic activity of histone deacetylases HDAC1, HDAC2 and HDAC3 (Class I) and HDAC6 (Class II) at nanomolar concentrations (IC50 less than 86 nM).
However, if either Rev-erb or HDAC3 is prevented from doing its job, the cycles do not occur, and the liver fills with fat.
Based on in vitro studies, ZOLINZA inhibits the enzymatic activity of HDAC1, HDAC2, HDAC3 (Class I) and HDAC 6 (class II) at nanomolar concentrations (IC50<86 nM).
They then engineered a mutation into mice that prevents NCoR from working with an enzyme that is normally its partner, HDAC3.
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