Synip CRISPR/Cas9 KO Plasmid (m): sc-423213
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- Synip 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 Synip 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 | |
Synip CRISPR/Cas9 KO Plasmid (m) | sc-423213 | 20 µg | $397.00 |
Overview
Stxbp4 encodes synaptotagmin-binding protein 4 (Synip), a syntaxin-interacting protein that participates in regulated vesicle trafficking and membrane fusion. Synip has been linked to insulin-stimulated GLUT4 vesicle translocation, supporting glucose uptake by coordinating SNARE-dependent docking and fusion events at the plasma membrane. Through its interactions with core exocytic machinery, Synip contributes to stimulus-coupled secretion and endomembrane dynamics that intersect with metabolic signaling pathways. Altered Synip function has been associated with impaired insulin responsiveness and broader defects in vesicle transport processes relevant to metabolic disease research.
Synip CRISPR/Cas9 KO Plasmid (m) is a pool of plasmids designed for targeted disruption of the Stxbp4 gene in mouse cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the Stxbp4 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 Stxbp4 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 Synip protein expression.
This CRISPR knockout system enables efficient generation of Stxbp4-deficient cell models for investigation of Synip signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.
Key Features
- sgRNAs targeting Stxbp4 exon(s) critical for Synip 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 Stxbp4 genomic sites to improve knockout efficiency
- Compatible with delivery by transfection
Design Variants
CRISPRs +/- HDRs
- gRNAs encoded by Synip CRISPR/Cas9 KO Plasmid (m) and Synip CRISPR/Cas9 KO Plasmid (m2) target distinct sites within the Stxbp4 locus. One or both targeting designs may be available. See Related Products for availability.
- HDR donor constructs encoded by Synip HDR Plasmid (m) and Synip HDR Plasmid (m2) contain a puromycin resistance cassette and an RFP reporter flanked by Stxbp4 homology arms to support homology-directed repair at defined Stxbp4 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.