HDAC2

HDAC2

A gene on chromosome 6q21 that encodes histone deacetylase 2, which belongs to the histone deacetylase family, which form large multiprotein complexes and adeacetylate lysine residues at the N-terminal regions of core histones (H2A, H2B, H3 and H4). HDAC2 forms transcriptional repressor complexes by associating with various proteins, including YY1—a mammalian zinc-finger transcription factor—MAD, SIN3 and N-COR; it plays a key role in transcription regulation, cell cycle progression and development.
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The fluorescent intensities of MRP2 in the control, HDAC2, and HDAC3 siRNA-transfected cells were week, and no significant differences were noticed among these three groups (all P > 0.
HDAC2 is a class-I enzyme (typically localizes to the cell nucleus) belonging to HDAC enzyme family which deacetylates histone tails and non-histone proteins changing chromatin structure (Montgomery et al.
HBI-8000 inhibits cancer-associated Class I HDAC1, HDAC2, HDAC3, as well as Class IIb HDAC10 at nanomolar concentrations and stimulates accumulation of acetylated histones H3 and H4 in tumor cells.
Primers of chromatin modifier genes were used, including the histone acetyltransferases (P300 and CREBBP) and the histone deacetylases (HDAC1, HDAC2, and HDAC7).
HDAC2 was generously provided by Ito Kazuhiro (Imperial College London), and PCAF, HMUF, and TIP60 were kindly provided by Bertrand Joseph (Karolinska Institutet) (see Supplemental Material, "Plasmids").
One study sponsored by the National Institutes of Health, for instance, found that a protein called HDAC2 forms in the brain during Alzheimer's and tightens up DNA strands, thereby locking the genes down and reducing their expression.
Researchers at Imperial College London found that children with severe asthma with a parent who smokes at home have lower levels of the enzyme HDAC2 compared with those whose parents don't smoke.
EZH2 supports nasopharyngeal carcinoma cell aggressiveness by forming a co-repressor complex with HDAC1/ HDAC2 and Snail to inhibit E-cadherin.
It is thought that these drugs improve steroid sensitivity by selective activation of histone deacetylase (HDAC) activity, in particular HDAC2, which suppresses inflammation in COPD.
Studies had shown that HDAC2 levels rise in the aging brain, even in healthy people.
Levels of HDAC2 are markedly unregulated in the aged mouse brain, the brain of several mouse models of Alzheimer's disease (AD), as well as in the human postmortem AD brain.
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.