twist Lentiviral Activation Particles (h): sc-400108-LAC
- Target species: human
- 200 µl of transduction-ready, high-titer CRISPR/dCas9 Lentiviral Activation Particles
- twist Lentiviral Activation Particles (h) is a synergistic activation mediator (SAM) transcription activation system designed to specifically and efficiently upregulate gene expression via lentiviral transduction of cells
- twist Lentiviral Activation Particles (h) contain the following SAM Activation elements: a deactivated Cas9 (dCas9) nuclease (D10A and N863A) fused to the transactivation domain VP64, an MS2-p65-HSF1 fusion protein and a target-specific 20 nt guide RNA. They also contain the blasticidin, hygromycin and puromycin resistance genes
- Upon transduction, the SAM complex binds to a site-specific region approximately 200-250 nt upstream of the transcriptional start site and provides robust recruitment of transcription factors for highly efficient gene activation
- gRNAs encoded by twist Lentiviral Activation Plasmid (h) and twist Lentiviral Activation Plasmid (h2) target distinct regulatory regions of the TWIST1 promoter. One or both designs may be available
- Following transfection, gene activation efficiency can be assayed by WB, IF or IHC using antibody: twist Antibody (Twist2C1a): sc-81417
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
twist Lentiviral Activation Particles (h) | sc-400108-LAC | 200 µl | $455.00 | |||
twist Lentiviral Activation Particles (h2) | sc-400108-LAC-2 | 200 µl | $455.00 |
TWIST1 encodes twist, a basic helix-loop-helix transcription factor that regulates mesenchymal lineage specification, morphogenesis, and epithelial–mesenchymal transition programs. Twist integrates developmental transcriptional networks with signaling pathways such as TGF-β, WNT/β-catenin, and PI3K/AKT to modulate cell fate decisions, survival, and motility-associated gene expression. Dysregulated TWIST1 expression is linked to altered differentiation states, invasiveness, and stem-like phenotypes across multiple cancer contexts, and germline disruption is associated with craniofacial developmental disorders including Saethre–Chotzen syndrome. These properties make TWIST1 a key node for studying transcriptional control of plasticity, lineage switching, and microenvironmental responses in human cells.
twist 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 TWIST1 upregulation across a broader range of human cell types.
twist 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 TWIST1 transcriptional start site, where VP64, p65, and HSF1 act cooperatively to recruit endogenous transcriptional machinery and drive sustained upregulation of endogenous twist expression. The use of nuclease-inactive dCas9 avoids the introduction of double-strand DNA breaks and preserves the native TWIST1 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.