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We used the following plasmids for transfections: HDAC1 (plasmid 13820), HDAC3 (plasmid 13819), and HDAC4 (plasmid 13821; all from Addgene).
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.
In this proposal, we plan to define the role of HDAC4 in muscle regeneration by identifying the targets responsible for the improved regeneration observed in HDAC4 null mice.
Importantly, the team also found that the two affected proteins interacted with one another; HDAC4 binds to ESRRA and inhibits it.
The fact that the HDAC4 mutation happens to increase the gene activity and happens to increase its ability to repress the ESSRA protein we found in the other family was just beyond coincidence," Lutter says.
16) In particular, the discovery that HD mice, engineered to be deficient in HDAC4, show a phenotypic improvement suggests that this may be a promising therapeutic approach.
The Mammalian HDAC enzymes The Class I HDACs -HDAC1 and HDAC2 -HDAC3 -HDAC8 -HDAC11 The Class II HDACs - HDAC4 and HDAC5 - HDAC6 - HDAC7 - HDAC9 - HDAC10 The Class III HDACs 7.
Our results showed that inhibition of NADPH oxidase activity ameliorated cerebral ischaemia/reperfusion (I/R) injury and among Zn(2+) -dependent HDACs, HDAC4 and HDAC5 were significantly decreased both in vivo and in vitro, which can be reversed by NADPH oxidase inhibitor apocynin.
The researchers found that HDAC4 is critically involved in regulating genes essential for communication between neurons.
We found that HDAC4 represses these genes, and its function in a given neuron is controlled by activity of other neurons forming a circuit," said TSRI Assistant Professor Anton Maximov, senior investigator for the study.
Richard Sando III, a graduate student at the TSRI Kellogg School of Science and Technology, a member of the Maximov lab and the first author of this study, noted the team become interested in class IIa histone deacetylases (HDACs), which include HDAC4, in part because they have been implicated in regulation of transcription of non-neuronal tissues.
Two of the new loci are in or near histone deacetylase genes HDAC4 and HDAC9.
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