Date published: 2026-9-3

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TMED9 CRISPR/Cas9 KO Plasmid (h): sc-407215

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Datasheets
  • Target species: human
  • 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
  • TMED9 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 TMED9 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

    TMED9 CRISPR/Cas9 KO Plasmid (h)

    sc-407215
    20 µg
    $397.00

    Overview

    TMED9 (p24 family member 9) encodes a type I transmembrane cargo receptor of the p24/TMED family that resides predominantly in the early secretory pathway. TMED9 participates in COPI- and COPII-dependent vesicular transport, supporting cargo selection and trafficking between the endoplasmic reticulum, ER–Golgi intermediate compartment, and Golgi, and contributes to organelle homeostasis and protein quality control. Through these roles, TMED9 influences secretion dynamics and intracellular distribution of membrane and secreted proteins, processes tightly linked to ER stress responses and proteostasis. Dysregulated secretory trafficking and ER–Golgi transport have been implicated in diverse human diseases, including cancer-associated remodeling of secretion and stress-adaptation pathways.

    TMED9 CRISPR/Cas9 KO Plasmid (h) is a pool of plasmids designed for targeted disruption of the TMED9 gene in human cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the TMED9 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 TMED9 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 TMED9 protein expression.

    This CRISPR knockout system enables efficient generation of TMED9-deficient cell models for investigation of TMED9 signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.

    Key Features

    • sgRNAs targeting TMED9 exon(s) critical for TMED9 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 TMED9 genomic sites to improve knockout efficiency
    • Compatible with delivery by transfection

    Design Variants

    CRISPRs +/- HDRs

    • gRNAs encoded by TMED9 CRISPR/Cas9 KO Plasmid (h) and TMED9 CRISPR/Cas9 KO Plasmid (h2) target distinct sites within the TMED9 locus. One or both targeting designs may be available. See Related Products for availability.
    • HDR donor constructs encoded by TMED9 HDR Plasmid (h) and TMED9 HDR Plasmid (h2) contain a puromycin resistance cassette and an RFP reporter flanked by TMED9 homology arms to support homology-directed repair at defined TMED9 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.