Seipin CRISPR/Cas9 KO Plasmid (m): sc-420617
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- Seipin 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 Seipin 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 | |
Seipin CRISPR/Cas9 KO Plasmid (m) | sc-420617 | 20 µg | $397.00 |
Overview
Mouse Bscl2 encodes seipin, an endoplasmic reticulum membrane protein that coordinates adipogenesis, lipid droplet biogenesis, and neutral lipid storage by regulating triglyceride and phospholipid flux at ER–lipid droplet junctions. Seipin supports proper lipid droplet morphology and limits aberrant accumulation of lipid intermediates that can perturb ER homeostasis and membrane composition. Disruption of seipin function is linked to lipodystrophy phenotypes and altered metabolic signaling, and it has also been associated with neurodegenerative processes in specific genetic contexts. Bscl2 therefore serves as a useful node for studying lipid homeostasis pathways, organelle contact sites, and cell type–specific metabolic vulnerability in mouse models.
Seipin CRISPR/Cas9 KO Plasmid (m) is a pool of plasmids designed for targeted disruption of the Bscl2 gene in mouse cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the Bscl2 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 Bscl2 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 Seipin protein expression.
This CRISPR knockout system enables efficient generation of Bscl2-deficient cell models for investigation of Seipin signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.
Key Features
- sgRNAs targeting Bscl2 exon(s) critical for Seipin 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 Bscl2 genomic sites to improve knockout efficiency
- Compatible with delivery by transfection
Design Variants
CRISPRs +/- HDRs
- gRNAs encoded by Seipin CRISPR/Cas9 KO Plasmid (m) and Seipin CRISPR/Cas9 KO Plasmid (m2) target distinct sites within the Bscl2 locus. One or both targeting designs may be available. See Related Products for availability.
- HDR donor constructs encoded by Seipin HDR Plasmid (m) and Seipin HDR Plasmid (m2) contain a puromycin resistance cassette and an RFP reporter flanked by Bscl2 homology arms to support homology-directed repair at defined Bscl2 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.