LSECtin CRISPR/Cas9 KO Plasmid (h): sc-404538
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- LSECtin CRISPR/Cas9 Knockout (KO) Plasmid (h) is a pool of plasmids, each encoding Cas9 nuclease and a target-specific 20 nt guide RNA (gRNA) designed for maximum knockout efficiency using sequences derived from the GeCKO v2 library
- gRNA sequences direct Cas9 to induce site-specific double-strand breaks (DSBs) in the LSECtin genomic locus, resulting in gene knockout through non-homologous end joining (NHEJ)
- The puromycin resistance and RFP genes are flanked by LoxP sites, enabling removal of selection markers via Cre recombinase (Cre Vector: sc-418923) after establishing stable knockout cell lines
- Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: LSECtin Antibody (SOTO-1): sc-65478
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
LSECtin CRISPR/Cas9 KO Plasmid (h) | sc-404538 | 20 µg | $397.00 |
Overview
CLEC4G encodes LSECtin, a C-type lectin receptor predominantly expressed by liver sinusoidal endothelial cells that binds specific glycan motifs on circulating glycoproteins and select pathogens. Through carbohydrate-recognition–dependent interactions, LSECtin contributes to hepatic immune surveillance, cell–cell adhesion, and modulation of leukocyte trafficking within the liver microenvironment. Reported signaling crosstalk includes regulation of antigen capture and processing pathways and coordination with other lectin and scavenger receptor networks that shape tolerogenic versus inflammatory responses. Dysregulated CLEC4G/LSECtin expression has been associated with altered tumor–liver interactions and immune evasion phenotypes, supporting its use as a mechanistic node in studies of hepatic inflammation, infection biology, and metastasis-related processes.
LSECtin CRISPR/Cas9 KO Plasmid (h) is a pool of plasmids designed for targeted disruption of the CLEC4G gene in human cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the CLEC4G 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 CLEC4G 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 LSECtin protein expression.
This CRISPR knockout system enables efficient generation of CLEC4G-deficient cell models for investigation of LSECtin signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.
Key Features
- sgRNAs targeting CLEC4G exon(s) critical for LSECtin 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 CLEC4G genomic sites to improve knockout efficiency
- Compatible with delivery by transfection
Design Variants
CRISPRs +/- HDRs
- gRNAs encoded by LSECtin CRISPR/Cas9 KO Plasmid (h) and LSECtin CRISPR/Cas9 KO Plasmid (h2) target distinct sites within the CLEC4G locus. One or both targeting designs may be available. See Related Products for availability.
- HDR donor constructs encoded by LSECtin HDR Plasmid (h) and LSECtin HDR Plasmid (h2) contain a puromycin resistance cassette and an RFP reporter flanked by CLEC4G homology arms to support homology-directed repair at defined CLEC4G 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.