L-Selectin/CD62L/SELL CRISPR Activation Plasmid (h): sc-401984-ACT

SELL encodes L-selectin (CD62L), an adhesion receptor expressed on leukocytes that mediates tethering and rolling on vascular endothelium through binding to sialylated, fucosylated ligands. This interaction coordinates lymphocyte homing to secondary lymphoid organs and regulates leukocyte trafficking during inflammation, integrating with chemokine-driven inside-out signaling and cytoskeletal remodeling to support extravasation. L-selectin shedding by metalloproteases further tunes cell migration and activation states, linking SELL expression dynamics to immune surveillance. Dysregulated CD62L levels or cleavage patterns are frequently studied in the context of inflammatory signaling, autoimmunity, and hematologic malignancy biology where altered trafficking impacts tissue infiltration.

L-Selectin/CD62L/SELL CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous SELL expression without altering the underlying DNA sequence.

L-Selectin/CD62L/SELL CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the SELL 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 SELL transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous L-Selectin/CD62L/SELL expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native SELL locus and enabling the study of L-Selectin/CD62L/SELL-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of L-Selectin/CD62L/SELL pathway restoration in tumor cells with silenced or reduced SELL expression.

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