P-Selectin/CD62P/SELP CRISPR/Cas9 KO Plasmid (h): sc-400441

Overview

SELP encodes P-selectin (CD62P), an inducible adhesion receptor stored in platelet α-granules and endothelial Weibel–Palade bodies and rapidly displayed on the cell surface after inflammatory or thrombotic stimulation. Surface P-selectin binds PSGL-1 on leukocytes to mediate tethering and rolling on activated endothelium and platelet–leukocyte interactions, coupling adhesion dynamics to downstream signaling that supports leukocyte recruitment and vascular inflammation. This axis intersects with selectin-mediated adhesion cascades, platelet activation, and coagulation-associated inflammatory pathways, shaping endothelial activation and immune cell trafficking. Dysregulated SELP expression or activity is frequently investigated in models of thrombosis, atherosclerosis, ischemia-reperfusion injury, and inflammatory disorders where platelet–endothelial–leukocyte crosstalk contributes to pathology.

P-Selectin/CD62P/SELP CRISPR/Cas9 KO Plasmid (h) is a pool of plasmids designed for targeted disruption of the SELP gene in human cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the SELP together with the Streptococcus pyogenes Cas9 nuclease. The plasmids also encode GFP, allowing fluorescent identification and enrichment of successfully transfected cells by fluorescence microscopy or flow cytometry.

The multi-guide design increases the likelihood of generating insertions or deletions (indels) that disrupt the SELP open reading frame following Cas9-mediated double-strand break formation. DNA breaks introduced by the CRISPR/Cas9 system are repaired through endogenous non-homologous end joining (NHEJ) pathways, frequently resulting in frameshift mutations that abolish P-Selectin/CD62P/SELP protein expression.

This CRISPR knockout system enables efficient generation of SELP-deficient cell models for investigation of P-Selectin/CD62P/SELP signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.

Key Features

• sgRNAs targeting SELP exon(s) critical for P-Selectin/CD62P/SELP function
• Co-expression of SpCas9 and sgRNA from a single plasmid for simplified delivery
• GFP reporter for identification of transfected cells
• Pool of plasmids targeting multiple SELP genomic sites to improve knockout efficiency
• Compatible with delivery by transfection

Design Variants

CRISPRs +/- HDRs

• gRNAs encoded by P-Selectin/CD62P/SELP CRISPR/Cas9 KO Plasmid (h) and P-Selectin/CD62P/SELP CRISPR/Cas9 KO Plasmid (h2) target distinct sites within the SELP locus. One or both targeting designs may be available. See Related Products for availability.
• HDR donor constructs encoded by P-Selectin/CD62P/SELP HDR Plasmid (h) and P-Selectin/CD62P/SELP HDR Plasmid (h2) contain a puromycin resistance cassette and an RFP reporter flanked by SELP homology arms to support homology-directed repair at defined SELP target sites corresponding to the CRISPR/Cas9 KO designs. HDR donor availability may vary. See Related Products for availability.

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