SLAM CRISPR Activation Plasmid (h): sc-404289-ACT

SLAMF1 encodes signaling lymphocytic activation molecule (SLAM, CD150), an immunoglobulin superfamily receptor expressed on multiple hematopoietic lineages that mediates homotypic cell–cell interactions. Upon engagement, SLAM couples to adaptor proteins such as SAP/SH2D1A and EAT-2 to modulate SRC-family kinase signaling, shaping lymphocyte activation, cytokine production, and germinal center responses. This receptor integrates into immune synapse organization and NF-κB/MAPK-associated signaling programs that influence effector differentiation and cytotoxic function. Dysregulated SLAMF1 signaling has been implicated in immune dysfunction and inflammatory pathophysiology, supporting its use as a target for mechanistic studies of immune regulation.

SLAM CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous SLAMF1 expression without altering the underlying DNA sequence.

SLAM CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the SLAMF1 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 SLAMF1 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous SLAM expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native SLAMF1 locus and enabling the study of SLAM-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of SLAM pathway restoration in tumor cells with silenced or reduced SLAMF1 expression.

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