β3Gn-T2 CRISPR/Cas9 KO Plasmid (m): sc-424741
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- β3Gn-T2 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 β3Gn-T2 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 | |
β3Gn-T2 CRISPR/Cas9 KO Plasmid (m) | sc-424741 | 20 µg | $397.00 |
Overview
B3gnt2 encodes β3Gn-T2, a Golgi-resident β1,3-N-acetylglucosaminyltransferase that extends poly-N-acetyllactosamine chains on N- and O-glycans and glycosphingolipids. By shaping glycan branching and elongation, β3Gn-T2 influences lectin-mediated recognition events, including galectin binding, which can affect cell adhesion, migration, and receptor organization at the plasma membrane. B3gnt2-dependent glycosylation contributes to regulation of immune and inflammatory signaling and modulates the composition of the glycocalyx in multiple tissues. Altered expression or activity of β3Gn-T family enzymes has been linked in the literature to dysregulated cell–cell interactions and phenotypes relevant to tumor biology and immune dysfunction, supporting mechanistic studies in mouse models.
β3Gn-T2 CRISPR/Cas9 KO Plasmid (m) is a pool of plasmids designed for targeted disruption of the B3gnt2 gene in mouse cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the B3gnt2 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 B3gnt2 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 β3Gn-T2 protein expression.
This CRISPR knockout system enables efficient generation of B3gnt2-deficient cell models for investigation of β3Gn-T2 signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.
Key Features
- sgRNAs targeting B3gnt2 exon(s) critical for β3Gn-T2 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 B3gnt2 genomic sites to improve knockout efficiency
- Compatible with delivery by transfection
Design Variants
CRISPRs +/- HDRs
- gRNAs encoded by β3Gn-T2 CRISPR/Cas9 KO Plasmid (m) and β3Gn-T2 CRISPR/Cas9 KO Plasmid (m2) target distinct sites within the B3gnt2 locus. One or both targeting designs may be available. See Related Products for availability.
- HDR donor constructs encoded by β3Gn-T2 HDR Plasmid (m) and β3Gn-T2 HDR Plasmid (m2) contain a puromycin resistance cassette and an RFP reporter flanked by B3gnt2 homology arms to support homology-directed repair at defined B3gnt2 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.