
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
Scleraxis Lentiviral Activation Particles (m) | sc-422833-LAC | 200 µl | $455.00 |
Mouse Scx encodes scleraxis, a basic helix–loop–helix transcription factor that functions as a lineage determinant for tendon and ligament fibroblasts and regulates extracellular matrix gene programs, including fibrillar collagens and proteoglycans. Scleraxis integrates mechanotransduction and TGF-β/BMP signaling to control tenocyte differentiation, matrix remodeling, and tissue maturation during development and repair. Altered Scx activity is associated with disrupted tendon homeostasis, impaired enthesis formation, and fibrotic remodeling processes that are relevant to musculoskeletal degeneration and abnormal connective tissue architecture. As a transcriptional regulator of ECM organization, scleraxis is widely studied in models of tendon injury, fibrosis, and stromal cell fate specification.
Scleraxis Lentiviral Activation Particles (m) address this need by packaging the complete synergistic activation mediator (SAM) transcriptional activation system into transduction-ready, high-titer lentiviral particles, enabling efficient Scx upregulation across a broader range of human cell types.
Scleraxis Lentiviral Activation Particles (m) 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 Scx transcriptional start site, where VP64, p65, and HSF1 act cooperatively to recruit endogenous transcriptional machinery and drive sustained upregulation of endogenous Scleraxis expression. The use of nuclease-inactive dCas9 avoids the introduction of double-strand DNA breaks and preserves the native Scx 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.