Histone Deacetylase 9 (HDAC9) CRISPR Activation Plasmid (m): sc-429766-ACT

Hdac9 encodes histone deacetylase 9 (HDAC9), a class IIa HDAC that acts as an epigenetic regulator linking signaling cues to chromatin state and transcriptional programs. HDAC9 shuttles between cytoplasm and nucleus and commonly functions within corepressor complexes to modulate histone acetylation and gene expression, influencing processes such as cell differentiation, metabolism, inflammatory signaling, and stress responses. In mouse systems, altered Hdac9 activity is frequently studied in the context of immune-cell function, cardiac and skeletal muscle remodeling, and neuronal plasticity, where HDAC9-dependent transcriptional rewiring can affect phenotype. Dysregulated HDAC9-associated pathways are relevant to mechanistic research on cardiometabolic traits, fibrosis, and neuroinflammation without implying therapeutic outcomes.

Histone Deacetylase 9 (HDAC9) CRISPR Activation Plasmid (m) provides a targeted, non-destructive approach to upregulating endogenous Hdac9 expression without altering the underlying DNA sequence.

Histone Deacetylase 9 (HDAC9) CRISPR Activation Plasmid (m) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the Hdac9 locus in human cell lines. The system is built around a catalytically inactive Cas9 (dCas9) carrying two inactivating mutations (D10A and N863A) that eliminate nuclease activity while preserving DNA binding. This dCas9 is fused to VP64, a potent transcriptional activator, and is co-expressed with a blasticidin resistance gene for selection. The second plasmid encodes the MS2-p65-HSF1 fusion protein, a secondary activator complex that works in concert with dCas9-VP64, alongside a hygromycin resistance gene. The third plasmid encodes a target-specific 20 nt sgRNA fused to two MS2 RNA aptamers that recruit the MS2-p65-HSF1 complex to the activation site, accompanied by a puromycin resistance gene. The three plasmids are delivered at a 1:1:1 mass ratio for balanced expression of all system components.

Once assembled at the target locus, the SAM complex binds within approximately 200 bp upstream of the Hdac9 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous Histone Deacetylase 9 (HDAC9) expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native Hdac9 locus and enabling the study of Histone Deacetylase 9 (HDAC9)-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of Histone Deacetylase 9 (HDAC9) pathway restoration in tumor cells with silenced or reduced Hdac9 expression.

For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.