HDAC8

HDAC8

A gene on chromosome Xq13 that encodes histone deacetylase 8, which belongs to class I of the histone deacetylase family; it catalyses the deacetylation of lysine residues and represses transcription in large multiprotein complexes with transcription co-repressors.
References in periodicals archive ?
(58) outlined the synthesis, characterization, and biological evaluation of suberoylanilide hydroxamic acid (SAHA)-based derivatives with greater binding towards HDAC8 than the SAHA.
CdLS is a rare multisystem genetic disease mainly caused by the mutations of genes code for cohesion system including SMC1A , SMC3 , RAD21 , NIPBL , and HDAC8 .[1] Cohesion plays a key role in the maintenance of genomic stability, as it is involved in the regulation of gene expressing, DNA repair, sister chromatid cohesion, chromatin remodeling, and long-range gene interactions.
Hsiao, "The novel HDAC8 inhibitor WK2-16 attenuates lipopolysaccharide-activated matrix metalloproteinase-9 expression in human monocytic cells and improves hypercytokinemia in vivo," International Journal of Molecular Sciences, vol.
The primers used were HDAC1: forward 5'-AGACAGCTGTGGCCCTGGA TAC-3' and reverse 5'-CGGCAGCATTCTAAGGTTCTC AA-3', HDAC2: forward 5'-TGCAGTTGCCCTTGATTGT GA-3' and reverse 5'-ATCTGGACACCAGGTGCATGAG3', HDAC3: forward 5'-AGAGTGGCCGCTACTACTGTC TGAA-3' and reverse 5'-TGGGTTGGTAGAAGTCCAC TACCTG-3', HDAC8: forward 5'-TGACGGAATGTGCA AAGTAGCAA-3' and reverse 5'-TCAAATTTCCGTCGCA ATCGTA-3', and GAPDH: forward 5'-GTGAACCATGA GAAGTATGACAAC-3' and reverse 5'-CATGAGTCCTT CCACGATACC-3'.
Mutations in the NIPBL, SMC1A, SMC3, RAD21, and HDAC8 genes have been identified to cause CdLS (4).
HDACs can be divided into four distinct families, of particular interest are class I (HDAC1, HDAC2, HDAC5, and HDAC8) and class II (HDAC5, HDAC6, HDAC7, HDAC9, and HDAC10) HDACs [26].
In accordance with their structural diversity, HDACs are divided into four subtypes: Class I (HDAC1, HDAC2, HDAC3, and HDAC8), Class II consisting of IIa (HDAC4, HDAC5, HDAC7, and HDAC9) and IIb (HDAC6 and HDAC10), Class III (a family of sirtuins), and Class IV (HDAC11) [4].
While direct association with HDACs 1-3 is observed with all MTG family members, the ability to interact with HDAC6 and HDAC8 is unique to MTG16 [36].
Another study in order to synthesize novel 6-(4-(4- aminophenylsulfonyl)phenylamino)-5H- benzo[a]phenoxazin-5-one derivatives has been published in addition to their molecular docking study with histone deacetylase (HDAC8) and cytotoxicity against cervical cancer cell line.
Pharmacophore model on histone deacetylase (HDAC8) with known hydroxamic acids has shown four pharmacophore features: one hydrogen acceptor, two hydrogen donors, and one hydrophobic group [18].
HDAC6 and HDAC8 enzyme activities contribute to cardiac hypertrophy and fibrosis in the heart obtained from chronic hypertensive rats [88].