Nanog Lentiviral Activation Particles (h): sc-418033-LAC

NANOG encodes the homeobox transcription factor Nanog, a central regulator of pluripotency that maintains self-renewal and suppresses lineage commitment in human stem cell states. Nanog cooperates with core transcriptional networks involving OCT4/POU5F1 and SOX2 and interfaces with signaling pathways such as TGF-β/SMAD, WNT/β-catenin, and FGF/ERK to balance pluripotent versus differentiated programs. Dysregulated NANOG expression is frequently used as a molecular readout of stemness and cellular plasticity, and altered NANOG-driven transcriptional circuits are studied in developmental defects and in tumor biology where stem-like phenotypes are implicated in progression and resistance mechanisms. As a nuclear DNA-binding protein, Nanog influences chromatin accessibility and transcriptional enhancer activity, making it a key node for mechanistic studies of gene regulatory networks.

Nanog 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 NANOG upregulation across a broader range of human cell types.

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