HDAC5

HDAC5

A gene on chromosome 17q21 that encodes histone deacetylase 5; it belongs to class II of the histone deacetylase/acuc/apha family, which has histone deacetylase activity and represses transcription when tethered to a promoter. HDAC5 acts indirectly via myocyte enhancer factor-2 (MEF2 proteins), repressing MEF2-dependent genes.
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Molecular mechanism of transcriptional repression of AhR repressor involving ANKRA2, HDAC4, and HDAC5.
The wild-type and mutation-type allele frequencies of the 15 SNPs identified in the genes DNMT1, DNMT3a, DNMT3b, Ago2, HDAC5, CAPN1, and PRKAG3 in all 14 breeds of cattle are shown in Figure 2.
Moreover, seven SNPs in the 5 genes (DNMT3L, AGO1, AGO2, HDAC5, and PRKAG3) were non-significantly associated with all of the beef carcass and quality traits in the Snow Dragon beef population.
Tenders are invited for Supply of Anti-bodies ERK/P-ERK, GRP78/BiP, HDAC5, GSK-3B, B-actin, Flag
Andre Fischer of the University of Gottingen in Germany says that inhibiting certain histone deacetylase enzymes, such as HDAC5, can make memory problems worse.
Simultaneously, antidepressant treatment reduced the expression of HDAC5, but when the levels of HDAC5 were elevated through genetic engineering, the effects of antidepressant treatment were reduced (Tsankova et al.
In contrast to the hippocampus, HDAC2 and HDAC5 levels in the NAc were reduced by chronic stress, suggesting opposing roles for histone modifications in the hippocampus and NAc in stress-related dysphoria (Renthal et al.
This mechanism involves cellular regulation of two proteins called HDAC5 and Cdk5, when SMN is lowered.
HDAC5 emerges, thus, as an epigenetic regulator that is involved in the transition between short-term physiological responses and long-term pathological states, with implications for the understanding of biological changes that occur during addiction and emotional stress.
The playbook begins with a key protein, histone deacetylase 5, or HDAC5, one of several proteins that influences gene expression - the process by which genes are turned on and converted into proteins that carry out the body's functions.
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.
In fact, the researchers found that bullied mice on imipramine made less of an enzyme called histone deacetylase 5 (HDACS), but mice in the no-stress group had normal levels of HDAC5 even after taking the antidepressant.