YAP Lentiviral Activation Particles (h): sc-400040-LAC

Human YAP1 encodes YAP, a transcriptional co-activator that functions as a key nuclear effector of the Hippo signaling pathway to regulate cell proliferation, survival, and organ size control. YAP activity is governed by phosphorylation-dependent cytoplasmic sequestration and nuclear shuttling, integrating mechanical cues, cell density, and GPCR signaling to modulate TEAD-driven gene expression programs. Dysregulated YAP1/YAP signaling has been implicated in altered tissue growth control, epithelial–mesenchymal programs, and changes in stem-like properties, making it a widely used node for studying growth-regulatory networks. In biomedical research, YAP is frequently examined for its roles in mechanotransduction, contact inhibition, and transcriptional reprogramming across diverse cell contexts.

YAP 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 YAP1 upregulation across a broader range of human cell types.

YAP 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 YAP1 transcriptional start site, where VP64, p65, and HSF1 act cooperatively to recruit endogenous transcriptional machinery and drive sustained upregulation of endogenous YAP expression. The use of nuclease-inactive dCas9 avoids the introduction of double-strand DNA breaks and preserves the native YAP1 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.