PATZ1 Lentiviral Activation Particles (h): sc-404881-LAC

PATZ1 (POZ/BTB and AT-hook-containing zinc finger 1) is a nuclear transcription factor that binds AT-rich DNA and interfaces with chromatin regulatory complexes to modulate gene expression programs controlling proliferation, differentiation, and apoptosis. Through its BTB/POZ domain and zinc-finger DNA-binding modules, PATZ1 participates in transcriptional repression and activation, influencing cell-cycle control, lineage commitment, and stress-responsive pathways. Altered PATZ1 expression or function has been associated with oncogenic and developmental phenotypes, including dysregulated transcriptional networks that impact tumor biology and cellular plasticity. As a context-dependent regulator, PATZ1 provides a useful entry point for dissecting transcription factor–driven circuitry, epigenetic control, and gene network robustness in human cells.

PATZ1 Lentiviral Activation Particles (h) address this need by packaging the complete synergistic activation mediator (SAM) transcriptional activation system into transduction-ready, high-titer lentiviral particles, enabling efficient PATZ1 upregulation across a broader range of human cell types.

PATZ1 Lentiviral Activation Particles (h) 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 PATZ1 transcriptional start site, where VP64, p65, and HSF1 act cooperatively to recruit endogenous transcriptional machinery and drive sustained upregulation of endogenous PATZ1 expression. The use of nuclease-inactive dCas9 avoids the introduction of double-strand DNA breaks and preserves the native PATZ1 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.