SLAMF6 CRISPR Activation Plasmid (h): sc-409009-ACT

SLAMF6 (signaling lymphocytic activation molecule family member 6, also known as NTB-A/CD352) is an immunoglobulin superfamily receptor expressed predominantly on T cells, NK cells, and subsets of B cells, where it functions as a homophilic co-receptor that tunes activation thresholds and effector programs. Through SLAM-associated adaptor signaling, including SAP/SH2D1A-dependent pathways, SLAMF6 influences proximal tyrosine phosphorylation events and downstream transcriptional outputs that shape cytokine production, cytotoxicity, and lymphocyte cross-talk. Altered SLAMF6 signaling has been linked to dysregulated immune homeostasis and immune-mediated pathology, and it is frequently examined in contexts of chronic inflammation, infection, and tumor immunology. As a surface checkpoint-like modulator of lymphocyte function, SLAMF6 is widely used as a mechanistic node for studying receptor co-stimulation, exhaustion-associated states, and lineage-specific immune signaling networks.

SLAMF6 CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous SLAMF6 expression without altering the underlying DNA sequence.

SLAMF6 CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the SLAMF6 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 SLAMF6 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous SLAMF6 expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native SLAMF6 locus and enabling the study of SLAMF6-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of SLAMF6 pathway restoration in tumor cells with silenced or reduced SLAMF6 expression.

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