Date published: 2026-9-3

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COG7 CRISPR/Cas9 KO Plasmid (h): sc-409352

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Datasheets
  • Target species: human
  • 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
  • COG7 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 COG7 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
  • Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: COG7 Antibody (G-1): sc-271699
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    Ordering Information

    Product NameCatalog #UNITPriceQtyFAVORITES

    COG7 CRISPR/Cas9 KO Plasmid (h)

    sc-409352
    20 µg
    $397.00

    Overview

    COG7 encodes a core subunit of the conserved oligomeric Golgi (COG) tethering complex, which supports intra-Golgi retrograde vesicle trafficking required for maintaining Golgi architecture and enzyme localization. By coordinating vesicle capture and fusion with Golgi membranes, COG7 helps ensure proper processing and sorting of secretory and membrane proteins, including glycosylation-dependent maturation steps. Disruption of COG7 function perturbs Golgi homeostasis and can lead to broad defects in protein glycosylation and trafficking, processes central to cell surface receptor regulation, secretion, and organelle communication. Variants in COG7 have been associated with congenital disorders of glycosylation, highlighting the gene’s relevance for studying glycoprotein biosynthesis and Golgi-related disease mechanisms.

    COG7 CRISPR/Cas9 KO Plasmid (h) is a pool of plasmids designed for targeted disruption of the COG7 gene in human cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the COG7 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 COG7 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 COG7 protein expression.

    This CRISPR knockout system enables efficient generation of COG7-deficient cell models for investigation of COG7 signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.

    Key Features

    • sgRNAs targeting COG7 exon(s) critical for COG7 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 COG7 genomic sites to improve knockout efficiency
    • Compatible with delivery by transfection

    Design Variants

    CRISPRs +/- HDRs

    • gRNAs encoded by COG7 CRISPR/Cas9 KO Plasmid (h) and COG7 CRISPR/Cas9 KO Plasmid (h2) target distinct sites within the COG7 locus. One or both targeting designs may be available. See Related Products for availability.
    • HDR donor constructs encoded by COG7 HDR Plasmid (h) and COG7 HDR Plasmid (h2) contain a puromycin resistance cassette and an RFP reporter flanked by COG7 homology arms to support homology-directed repair at defined COG7 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.