RADX Lentiviral Activation Particles (h): sc-409991-LAC
- Target species: human
- 200 µl of transduction-ready, high-titer CRISPR/dCas9 Lentiviral Activation Particles
- RADX 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
- RADX 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 RADX Lentiviral Activation Plasmid (h) and RADX Lentiviral Activation Plasmid (h2) target distinct regulatory regions of the CXorf57 promoter. One or both designs may be available
- Following transfection, gene activation efficiency can be assayed by WB, IF or IHC using antibody: RADX Antibody (A-3): sc-514563
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
RADX Lentiviral Activation Particles (h) | sc-409991-LAC | 200 µl | $455.00 |
Human CXorf57 encodes RADX, a single-stranded DNA–binding factor that regulates replication fork dynamics and genome stability. RADX modulates RAD51 loading at stalled forks, helping balance fork protection, restart, and repriming during replication stress, and it interfaces with ATR-dependent DNA damage signaling and homologous recombination control. Through these functions, RADX contributes to suppression of aberrant recombination and maintenance of chromosome integrity, making it relevant to studies of replication stress phenotypes, mutational processes, and genome instability observed across diverse disease contexts.
RADX 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 CXorf57 upregulation across a broader range of human cell types.
RADX 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 CXorf57 transcriptional start site, where VP64, p65, and HSF1 act cooperatively to recruit endogenous transcriptional machinery and drive sustained upregulation of endogenous RADX expression. The use of nuclease-inactive dCas9 avoids the introduction of double-strand DNA breaks and preserves the native CXorf57 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.