CLEC-2B CRISPR/Cas9 KO Plasmid (m): sc-425297
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- CLEC-2B CRISPR/Cas9 Knockout (KO) Plasmid (m) 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 CLEC-2B 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
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
CLEC-2B CRISPR/Cas9 KO Plasmid (m) | sc-425297 | 20 µg | $397.00 |
Overview
Clec1b encodes the mouse C-type lectin receptor CLEC-2B, a type II membrane protein implicated in ligand-dependent signaling at the cell surface. As a member of the C-type lectin-like receptor family, CLEC-2B contributes to regulation of immune and vascular-related cellular communication by modulating receptor-mediated activation and downstream phosphorylation cascades. Functional links to platelet-associated signaling networks and inflammatory microenvironments make Clec1b relevant for studies of hemostasis, leukocyte–endothelium interactions, and tissue remodeling. Dysregulated lectin receptor signaling is frequently investigated in the context of thrombosis-associated inflammation and immune-driven pathology using mechanistic mouse models.
CLEC-2B CRISPR/Cas9 KO Plasmid (m) is a pool of plasmids designed for targeted disruption of the Clec1b gene in mouse cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the Clec1b 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 Clec1b 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 CLEC-2B protein expression.
This CRISPR knockout system enables efficient generation of Clec1b-deficient cell models for investigation of CLEC-2B signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.
Key Features
- sgRNAs targeting Clec1b exon(s) critical for CLEC-2B 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 Clec1b genomic sites to improve knockout efficiency
- Compatible with delivery by transfection
Design Variants
CRISPRs +/- HDRs
- gRNAs encoded by CLEC-2B CRISPR/Cas9 KO Plasmid (m) and CLEC-2B CRISPR/Cas9 KO Plasmid (m2) target distinct sites within the Clec1b locus. One or both targeting designs may be available. See Related Products for availability.
- HDR donor constructs encoded by CLEC-2B HDR Plasmid (m) and CLEC-2B HDR Plasmid (m2) contain a puromycin resistance cassette and an RFP reporter flanked by Clec1b homology arms to support homology-directed repair at defined Clec1b 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.