CD44 Lentiviral Activation Particles (h): sc-400209-LAC

Human CD44 encodes a widely expressed transmembrane glycoprotein that serves as a principal receptor for hyaluronan and other extracellular matrix ligands, coordinating cell–cell and cell–matrix interactions. Through isoform-specific signaling and cytoskeletal coupling, CD44 influences adhesion, migration, lymphocyte homing, and epithelial–mesenchymal dynamics, integrating cues from the extracellular matrix with intracellular pathways such as Rho GTPase remodeling and receptor tyrosine kinase crosstalk. CD44 activity is frequently linked to inflammatory responses and tissue remodeling, and altered expression or splicing patterns have been associated with tumor invasion, metastasis-related phenotypes, and cancer stem-like cell properties. These features make CD44 a useful node for studying microenvironmental signaling, leukocyte trafficking, and extracellular matrix–driven regulation of gene expression.

CD44 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 CD44 upregulation across a broader range of human cell types.

CD44 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 CD44 transcriptional start site, where VP64, p65, and HSF1 act cooperatively to recruit endogenous transcriptional machinery and drive sustained upregulation of endogenous CD44 expression. The use of nuclease-inactive dCas9 avoids the introduction of double-strand DNA breaks and preserves the native CD44 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.