COG5 CRISPR/Cas9 KO Plasmid (h): sc-411474
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- COG5 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 COG5 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 | |
COG5 CRISPR/Cas9 KO Plasmid (h) | sc-411474 | 20 µg | $397.00 |
Overview
COG5 encodes a core subunit of the conserved oligomeric Golgi (COG) tethering complex that coordinates retrograde vesicle trafficking within the Golgi apparatus. By supporting vesicle docking and SNARE-dependent fusion, COG5 helps maintain Golgi architecture, enzyme localization, and efficient processing of secretory cargo. Disruption of COG complex function perturbs glycosylation homeostasis and can alter cell-surface and extracellular matrix composition, affecting pathways linked to protein sorting, secretion, and membrane organization. Variants in COG5 and related COG components have been associated with congenital disorders of glycosylation and broader phenotypes connected to defective Golgi trafficking.
COG5 CRISPR/Cas9 KO Plasmid (h) is a pool of plasmids designed for targeted disruption of the COG5 gene in human cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the COG5 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 COG5 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 COG5 protein expression.
This CRISPR knockout system enables efficient generation of COG5-deficient cell models for investigation of COG5 signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.
Key Features
- sgRNAs targeting COG5 exon(s) critical for COG5 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 COG5 genomic sites to improve knockout efficiency
- Compatible with delivery by transfection
Design Variants
CRISPRs +/- HDRs
- gRNAs encoded by COG5 CRISPR/Cas9 KO Plasmid (h) and COG5 CRISPR/Cas9 KO Plasmid (h2) target distinct sites within the COG5 locus. One or both targeting designs may be available. See Related Products for availability.
- HDR donor constructs encoded by COG5 HDR Plasmid (h) and COG5 HDR Plasmid (h2) contain a puromycin resistance cassette and an RFP reporter flanked by COG5 homology arms to support homology-directed repair at defined COG5 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.