Psychiatry related information on Setdb1

• ESET/SETDB1 gene expression and histone H3 (K9) trimethylation in Huntington's disease [1].

High impact information on Setdb1

• Quiescent B cells also lacked heterochromatin-associated HP1beta and Ikaros at pericentric chromatin and expressed low levels of Ezh2 and ESET histone methyl transferases (HMTases) [2].
• We show that ESET expression is markedly increased in HD patients and in transgenic R6/2 HD mice [1].
• ERG-associated protein with SET domain (ESET), a histone H3 (K9) methyltransferase, mediates histone methylation [1].
• Our data suggest that modulation of gene silencing mechanisms, through regulation of the ESET gene is important to neuronal survival and, as such, may be a promising treatment in HD patients [1].
• Blastocysts null for Eset were recovered but in less than Mendelian ratios [3].

Biological context of Setdb1

• The combined pharmacological treatment with mithramycin and cystamine down-regulates ESET gene expression and reduces hypertrimethylation of histone H3 (K9) [1].
• Global H3-K9 trimethylation and DNA methylation at IAP repeats in Eset(-/-) blastocyst outgrowths were not dramatically altered [3].
• The transcription initiation site of the ESET gene was determined by 5'-RACE experiment and by primer extension [4].
• The 5'-flanking sequence of the ESET gene does not contain the consensus TATA box [4].
• The ESET promoter was functionally active when tested in transfection and luciferase assay [4].

Other interactions of Setdb1

• We found that zygotic Eset expression begins at the blastocyst stage and is ubiquitous during postimplantation mouse development, while the maternal Eset transcripts are present in oocytes and persist throughout preimplantation development [3].

References