ZNF831 Lentiviral Activation Particles (h2): sc-414334-LAC-2

Human ZNF831 encodes a KRAB-containing C2H2 zinc finger protein that is predicted to function as a DNA-binding transcriptional regulator, coordinating gene-expression programs through sequence-specific promoter/enhancer interactions and recruitment of chromatin-modifying co-repressor complexes. Through these activities, ZNF831 is implicated in epigenetic control of cell-state decisions, immune-related transcriptional networks, and broader processes such as differentiation and inflammatory signaling. Genetic and expression studies have linked ZNF831 to immune-mediated disease susceptibility and dysregulated immune homeostasis, supporting its relevance for mechanistic investigations of autoimmunity-associated regulatory circuits. Targeted perturbation of ZNF831 enables researchers to dissect transcription factor–chromatin interactions, map downstream gene networks, and validate regulatory variants in human cellular models.

ZNF831 Lentiviral Activation Particles (h2) address this need by packaging the complete synergistic activation mediator (SAM) transcriptional activation system into transduction-ready, high-titer lentiviral particles, enabling efficient ZNF831 upregulation across a broader range of human cell types.

ZNF831 Lentiviral Activation Particles (h2) 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 ZNF831 transcriptional start site, where VP64, p65, and HSF1 act cooperatively to recruit endogenous transcriptional machinery and drive sustained upregulation of endogenous ZNF831 expression. The use of nuclease-inactive dCas9 avoids the introduction of double-strand DNA breaks and preserves the native ZNF831 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.