
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
IL-8RB CRISPR Activation Plasmid (h) | sc-401404-ACT | 20 µg | $397.00 | |||
IL-8RB CRISPR Activation Plasmid (h2) | sc-401404-ACT-2 | 20 µg | $397.00 |
CXCR2 encodes interleukin-8 receptor beta (IL-8RB), a seven-transmembrane GPCR that binds ELR+ CXC chemokines such as CXCL8/IL-8 to direct chemotaxis, adhesion, and activation of neutrophils and other myeloid cells. Receptor engagement triggers Gαi-dependent signaling that modulates intracellular calcium flux and activates MAPK/ERK, PI3K–AKT, and NF-κB pathways, shaping inflammatory gene expression and cytoskeletal remodeling. CXCR2 signaling coordinates leukocyte trafficking, angiogenic cues, and tissue responses to injury, and dysregulated chemokine receptor activity is implicated in chronic inflammation and tumor-associated immune cell recruitment. As a result, CXCR2/IL-8RB is widely studied in models of inflammatory microenvironments, myeloid cell biology, and chemokine-driven cell migration.
IL-8RB CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous CXCR2 expression without altering the underlying DNA sequence.
IL-8RB CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the CXCR2 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 CXCR2 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous IL-8RB expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native CXCR2 locus and enabling the study of IL-8RB-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of IL-8RB pathway restoration in tumor cells with silenced or reduced CXCR2 expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.