Date published: 2026-7-19

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AP1GBP1 CRISPR/Cas9 KO Plasmid (h): sc-411596

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Datasheets
  • Target species: human
  • 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
  • AP1GBP1 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 AP1GBP1 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
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    Ordering Information

    Product NameCatalog #UNITPriceQtyFAVORITES

    AP1GBP1 CRISPR/Cas9 KO Plasmid (h)

    sc-411596
    20 µg
    $397.00

    Overview

    SYNRG encodes AP1GBP1 (synergin gamma), an adaptor-associated protein implicated in clathrin-mediated trafficking and cargo sorting between the trans-Golgi network and endosomal compartments. AP1GBP1 interacts with the AP-1 adaptor complex and contributes to vesicle coat assembly, membrane curvature, and the spatial regulation of sorting signals that control protein localization. Through these functions, SYNRG supports secretory and endocytic pathway homeostasis, influencing receptor recycling, lysosomal targeting, and compartmental identity. Dysregulated intracellular trafficking is a recurrent feature of neurodevelopmental and neurodegenerative processes as well as oncogenic signaling rewiring, making SYNRG a useful node for mechanistic studies of pathway-dependent protein transport.

    AP1GBP1 CRISPR/Cas9 KO Plasmid (h) is a pool of plasmids designed for targeted disruption of the SYNRG gene in human cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the SYNRG 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 SYNRG 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 AP1GBP1 protein expression.

    This CRISPR knockout system enables efficient generation of SYNRG-deficient cell models for investigation of AP1GBP1 signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.

    Key Features

    • sgRNAs targeting SYNRG exon(s) critical for AP1GBP1 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 SYNRG genomic sites to improve knockout efficiency
    • Compatible with delivery by transfection

    Design Variants

    CRISPRs +/- HDRs

    • gRNAs encoded by AP1GBP1 CRISPR/Cas9 KO Plasmid (h) and AP1GBP1 CRISPR/Cas9 KO Plasmid (h2) target distinct sites within the SYNRG locus. One or both targeting designs may be available. See Related Products for availability.
    • HDR donor constructs encoded by AP1GBP1 HDR Plasmid (h) and AP1GBP1 HDR Plasmid (h2) contain a puromycin resistance cassette and an RFP reporter flanked by SYNRG homology arms to support homology-directed repair at defined SYNRG 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.