VPS26B CRISPR/Cas9 KO Plasmid (h): sc-410249
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- VPS26B 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 VPS26B 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 | |
VPS26B CRISPR/Cas9 KO Plasmid (h) | sc-410249 | 20 µg | $397.00 |
Overview
VPS26B encodes a core subunit of the retromer cargo-selective complex that regulates endosome-to-Golgi retrieval and endosomal recycling of transmembrane proteins. By coordinating cargo recognition with endosomal sorting machinery, VPS26B helps maintain receptor homeostasis, vesicle trafficking, and organelle integrity, processes that influence signaling amplitude and membrane protein turnover. Retromer-associated pathways intersect with autophagy, lysosomal function, and polarized transport, making VPS26B relevant for studying neuronal maintenance and general proteostasis. Dysregulated endosomal trafficking and retromer dysfunction have been linked to neurodegenerative and developmental phenotypes, supporting mechanistic investigation of VPS26B in disease-relevant cellular models.
VPS26B CRISPR/Cas9 KO Plasmid (h) is a pool of plasmids designed for targeted disruption of the VPS26B gene in human cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the VPS26B 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 VPS26B 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 VPS26B protein expression.
This CRISPR knockout system enables efficient generation of VPS26B-deficient cell models for investigation of VPS26B signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.
Key Features
- sgRNAs targeting VPS26B exon(s) critical for VPS26B 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 VPS26B genomic sites to improve knockout efficiency
- Compatible with delivery by transfection
Design Variants
CRISPRs +/- HDRs
- gRNAs encoded by VPS26B CRISPR/Cas9 KO Plasmid (h) and VPS26B CRISPR/Cas9 KO Plasmid (h2) target distinct sites within the VPS26B locus. One or both targeting designs may be available. See Related Products for availability.
- HDR donor constructs encoded by VPS26B HDR Plasmid (h) and VPS26B HDR Plasmid (h2) contain a puromycin resistance cassette and an RFP reporter flanked by VPS26B homology arms to support homology-directed repair at defined VPS26B 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.