
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
BTN3A1 CRISPR Activation Plasmid (h) | sc-404202-ACT | 20 µg | $397.00 |
BTN3A1 (butyrophilin subfamily 3 member A1, CD277) is a human immunoregulatory type I transmembrane protein that functions in antigen-sensing and T cell modulation, particularly influencing Vγ9Vδ2 T cell activation through phosphoantigen-dependent signaling. It participates in immune synapse organization and downstream pathways governing lymphocyte activation, cytokine production, and cytotoxic responses. BTN3A1 expression and signaling dynamics are frequently interrogated in tumor immunology and inflammatory biology, where altered regulation can reshape immune surveillance and cellular stress responses. As a cell-surface checkpoint-like mediator, BTN3A1 provides a tractable node for studying immune activation thresholds and immune–tumor interactions in vitro.
BTN3A1 CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous BTN3A1 expression without altering the underlying DNA sequence.
BTN3A1 CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the BTN3A1 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 BTN3A1 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous BTN3A1 expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native BTN3A1 locus and enabling the study of BTN3A1-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of BTN3A1 pathway restoration in tumor cells with silenced or reduced BTN3A1 expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.