Histone Deacetylase 1 (HDAC1) CRISPR Activation Plasmid (m): sc-436647-ACT

Histone deacetylase 1 (HDAC1), encoded by the mouse Hdac1 gene, is a class I lysine deacetylase that removes acetyl groups from histones and non-histone substrates to regulate chromatin accessibility and transcriptional programs. HDAC1 functions in multiprotein repressor complexes such as Sin3, NuRD, and CoREST to coordinate epigenetic silencing, cell-cycle progression, DNA replication, and differentiation decisions. Through crosstalk with DNA damage responses and replication stress pathways, HDAC1 helps shape genome stability and checkpoint control. Dysregulated HDAC1 activity and altered histone acetylation states are widely associated with aberrant transcriptional networks in cancer models, neurodevelopmental phenotypes, and inflammatory signaling, making it a key node for mechanistic epigenetics research.

Histone Deacetylase 1 (HDAC1) CRISPR Activation Plasmid (m) provides a targeted, non-destructive approach to upregulating endogenous Hdac1 expression without altering the underlying DNA sequence.

Histone Deacetylase 1 (HDAC1) CRISPR Activation Plasmid (m) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the Hdac1 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 Hdac1 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous Histone Deacetylase 1 (HDAC1) expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native Hdac1 locus and enabling the study of Histone Deacetylase 1 (HDAC1)-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of Histone Deacetylase 1 (HDAC1) pathway restoration in tumor cells with silenced or reduced Hdac1 expression.

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