HDAC9
HDAC9 (histone deacetylase 9, also known as MITR, HDAC7B, HD7 and KIAA0744) is a nuclear class IIA histone deacetylase family member that represses MEF2-dependent transcription. It has been linked to myogenesis, heart development, neuronal survival and haematopoiesis. Browse Assay Genie's current range of HDAC9 research reagents below, or read on for the biology behind the target.
HDAC9 belongs to the histone deacetylase family and sits in the HD type 2 subfamily, grouped by HGNC as class IIA histone deacetylases. Histone acetylation and deacetylation alter chromosome structure and affect how readily transcription factors reach DNA, so enzymes of this family contribute to transcriptional regulation, cell cycle progression and developmental events. HDAC9 acts mainly as a transcriptional corepressor. It represses MEF2-dependent transcription by recruiting HDAC1 and/or HDAC3, and NCBI notes that it also draws in multicomponent corepressor complexes that include CtBP and HDACs.
The HDAC9 gene encodes several alternatively spliced transcripts, and the full-length nature of some has not been determined. Isoform 3, the MITR form, lacks the active site residues and the histone deacetylase catalytic domain, so it is catalytically inactive. It works through corepressor recruitment rather than its own enzymatic activity. The gene is orthologous to the Xenopus and mouse MITR genes, and the mouse counterpart is Hdac9. Researchers studying the HDAC9 gene or HDAC9 protein often need to distinguish between these isoforms.
Functional annotation links HDAC9 to several biological settings. It seems to inhibit skeletal myogenesis and to be involved in heart development. It also protects neurons from apoptosis, both by inhibiting JUN phosphorylation by MAPK10 and by repressing JUN transcription through recruitment of HDAC1 to the JUN promoter. NCBI additionally suggests a role in haematopoiesis. Together these functions make HDAC9 a useful subject for work on epigenetic control of differentiation and cell survival.
HDAC9 represses MEF2-dependent transcription by recruiting HDAC1 and/or HDAC3, making it a model for corepressor-mediated gene regulation.
HDAC9 seems to inhibit skeletal myogenesis and to be involved in heart development, relevant to studies of differentiation programmes.
HDAC9 protects neurons from apoptosis by limiting JUN phosphorylation by MAPK10 and by repressing JUN transcription through HDAC1 recruitment.
NCBI Gene reports that the HDAC9 protein may play a role in haematopoiesis, supporting investigation of blood cell development.
HDAC9 is a nuclear transcriptional corepressor. It represses MEF2-dependent transcription by recruiting HDAC1 and/or HDAC3. It seems to inhibit skeletal myogenesis, is involved in heart development, and protects neurons from apoptosis by acting on JUN phosphorylation and JUN transcription.
HDAC9 is also called MITR, HDAC7B, HD7, HDAC and KIAA0744. Several alternatively spliced transcripts exist. Isoform 3, the MITR form, lacks the catalytic domain and active site residues, so it is catalytically inactive but still represses MEF2 through corepressor recruitment.
Yes. NCBI states that the gene is orthologous to the Xenopus and mouse MITR genes, and the mouse ortholog is Hdac9. Cross-species use of any reagent depends on its own validation, so check the datasheet of any product for its validated reactivity.
Other class IIA histone deacetylases, the HDAC1 and HDAC3 corepressors recruited by HDAC9, and further members of the HDAC family.
Gene and protein annotations from HGNC, NCBI Gene and UniProt Q9UKV0; product specifications from Assay Genie datasheets.