CXCR-7 CRISPR Activation Plasmid (h): sc-403187-ACT
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- CXCR-7 CRISPR Activation Plasmid (h) is a synergistic activation mediator (SAM) transcription activation system designed to specifically upregulate gene expression
- CXCR-7 CRISPR Activation Plasmid (h) consists of three plasmids at a 1:1:1 mass ratio: a plasmid encoding the deactivated Cas9 (dCas9) nuclease (D10A and N863A) fused to the transactivation domain VP64, and a blasticidin resistance gene; a plasmid encoding the MS2-p65-HSF1 fusion protein, and a hygromycin resistance gene; a plasmid encoding a target-specific 20 nt guide RNA fused to two MS2 RNA aptamers, and a puromycin resistance gene
- The resulting 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 CXCR-7 CRISPR Activation Plasmid (h) and CXCR-7 CRISPR Activation Plasmid (h2) target distinct regulatory regions upstream of the ACKR3 transcriptional start site. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
CXCR-7 CRISPR Activation Plasmid (h) | sc-403187-ACT | 20 µg | $397.00 |
ACKR3 (CXCR-7) encodes an atypical chemokine receptor that binds CXCL12/SDF-1 and CXCL11, functioning primarily as a ligand scavenger and signaling modulator rather than a canonical Gαi-coupled chemotactic receptor. By shaping chemokine gradients and receptor cross-talk, CXCR-7 influences CXCR4-dependent migration, survival, and adhesion programs and impacts downstream pathways including MAPK/ERK and β-arrestin–associated signaling. In human tissues, ACKR3 contributes to vascular and immune cell trafficking dynamics, with frequent investigation in contexts such as inflammation, tumor cell invasion, metastasis biology, and angiogenesis. Its expression and activity are also studied in development and tissue remodeling where chemokine availability is rate-limiting for cell positioning.
CXCR-7 CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous ACKR3 expression without altering the underlying DNA sequence.
CXCR-7 CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the ACKR3 locus in human cell lines. The system is built around a catalytically inactive Cas9 (dCas9) carrying two inactivating mutations (D10A and N863A) that eliminate nuclease activity while preserving DNA binding. This dCas9 is fused to VP64, a potent transcriptional activator, and is co-expressed with a blasticidin resistance gene for selection. The second plasmid encodes the MS2-p65-HSF1 fusion protein, a secondary activator complex that works in concert with dCas9-VP64, alongside a hygromycin resistance gene. The third plasmid encodes a target-specific 20 nt sgRNA fused to two MS2 RNA aptamers that recruit the MS2-p65-HSF1 complex to the activation site, accompanied by a puromycin resistance gene. The three plasmids are delivered at a 1:1:1 mass ratio for balanced expression of all system components.
Once assembled at the target locus, the SAM complex binds within approximately 200 bp upstream of the ACKR3 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous CXCR-7 expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native ACKR3 locus and enabling the study of CXCR-7-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of CXCR-7 pathway restoration in tumor cells with silenced or reduced ACKR3 expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.