Histone Deacetylase 1 (HDAC1) Lentiviral Activation Particles (m): sc-436647-LAC

Mouse Hdac1 encodes histone deacetylase 1 (HDAC1), a class I HDAC that removes acetyl groups from lysine residues on histones and other nuclear substrates to regulate chromatin accessibility and transcriptional programs. HDAC1 functions in multiprotein corepressor assemblies including SIN3, NuRD, and CoREST, linking it to cell-cycle control, DNA damage responses, and lineage-specific differentiation. Through coupling to transcription factors and chromatin remodelers, HDAC1 shapes epigenetic states that influence proliferation, apoptosis, and developmental gene expression. Dysregulated HDAC1 activity is frequently studied in contexts of oncogenic transcriptional repression, neurodevelopmental phenotypes, and immune cell activation states, making it a central node for epigenetics-driven disease mechanisms in mouse models.

Histone Deacetylase 1 (HDAC1) Lentiviral Activation Particles (m) address this need by packaging the complete synergistic activation mediator (SAM) transcriptional activation system into transduction-ready, high-titer lentiviral particles, enabling efficient Hdac1 upregulation across a broader range of human cell types.

Histone Deacetylase 1 (HDAC1) Lentiviral Activation Particles (m) deliver all functional components of the synergistic activation mediator (SAM) system via lentiviral transduction. The system comprises three particle preparations co-transduced into target cells: one encoding catalytically inactive dCas9 (D10A and N863A mutations) fused to the VP64 transactivation domain with a blasticidin resistance gene; one encoding the MS2-p65-HSF1 fusion protein with a hygromycin resistance gene; and one encoding a target-specific 20 nt sgRNA fused to two MS2 RNA aptamers with a puromycin resistance gene. Following lentiviral transduction and genomic integration of the expression cassettes, the SAM components are stably expressed and assemble at the target locus within the proximal promoter region upstream of the Hdac1 transcriptional start site, where VP64, p65, and HSF1 act cooperatively to recruit endogenous transcriptional machinery and drive sustained upregulation of endogenous Histone Deacetylase 1 (HDAC1) expression. The use of nuclease-inactive dCas9 avoids the introduction of double-strand DNA breaks and preserves the native Hdac1 genomic locus and regulatory architecture.

The lentiviral format offers several practical advantages: stable genomic integration supports heritable activation across cell divisions; high-titer particle preparations eliminate the need for in-house viral production; and compatibility with primary, non-dividing, and transfection-resistant cell types expands experimental accessibility. Successful transduction can be confirmed and enriched through triple antibiotic selection using puromycin, hygromycin, and blasticidin.

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