CS1 CRISPR Activation Plasmid (h): sc-401906-ACT

SLAMF7 (CS1) is a cell-surface immunoreceptor of the SLAM family expressed predominantly on natural killer cells and subsets of B-lineage and plasma cells, where it modulates immune synapse formation and effector programs. Through homotypic interactions and adaptor-dependent signaling, CS1 influences activation thresholds, cytokine secretion, and cytotoxic responses, integrating with pathways that control lymphocyte communication and immune surveillance. Dysregulated SLAMF7 expression has been associated with altered lymphoid cell behavior and tumor–immune interactions in hematologic malignancy contexts, making it a useful marker and functional node for studying immune regulation. Experimental perturbation of SLAMF7 supports mechanistic studies of immune-cell activation, receptor signaling networks, and microenvironment-dependent phenotypes.

CS1 CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous SLAMF7 expression without altering the underlying DNA sequence.

CS1 CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the SLAMF7 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 SLAMF7 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous CS1 expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native SLAMF7 locus and enabling the study of CS1-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of CS1 pathway restoration in tumor cells with silenced or reduced SLAMF7 expression.

For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.