
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
Cdx1 Lentiviral Activation Particles (h) | sc-402522-LAC | 200 µl | $455.00 |
Human CDX1 encodes the homeobox transcription factor Cdx1, a regulator of anterior–posterior patterning and intestinal epithelial differentiation. Cdx1 integrates developmental signaling inputs, including Wnt/β-catenin and BMP-related pathways, to control transcriptional programs governing proliferation, lineage specification, and maintenance of gut identity. Altered CDX1 expression has been associated with dysregulated epithelial maturation and intestinal metaplasia, and it is frequently studied in the context of colorectal tumor biology and mucosal disease mechanisms. As a DNA-binding transcriptional regulator, Cdx1 provides a tractable node for dissecting gene regulatory networks that shape epithelial fate and barrier-associated functions.
Cdx1 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 CDX1 upregulation across a broader range of human cell types.
Cdx1 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 CDX1 transcriptional start site, where VP64, p65, and HSF1 act cooperatively to recruit endogenous transcriptional machinery and drive sustained upregulation of endogenous Cdx1 expression. The use of nuclease-inactive dCas9 avoids the introduction of double-strand DNA breaks and preserves the native CDX1 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.