Date published: 2026-10-8

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TMEM182 CRISPR/Cas9 KO Plasmid (m): sc-436273

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Datasheets
  • Target species: mouse
  • 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
  • TMEM182 CRISPR/Cas9 Knockout (KO) Plasmid (m) 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 TMEM182 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

    TMEM182 CRISPR/Cas9 KO Plasmid (m)

    sc-436273
    20 µg
    $397.00

    Overview

    Tmem182 encodes TMEM182, a predicted multi-pass transmembrane protein with enriched expression in skeletal muscle and links to myogenic differentiation programs. Although its molecular function remains incompletely defined, TMEM182 has been associated with membrane-associated signaling and cellular remodeling processes that accompany muscle development and regeneration. Transcriptomic studies have reported Tmem182 regulation in contexts involving metabolic adaptation and inflammatory cues, suggesting relevance to pathways that shape muscle homeostasis and stress responses. Dysregulated expression has been observed in muscle-related phenotypes and experimental models of tissue remodeling, supporting its use as a target for mechanistic studies in musculoskeletal biology.

    TMEM182 CRISPR/Cas9 KO Plasmid (m) is a pool of plasmids designed for targeted disruption of the Tmem182 gene in mouse cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the Tmem182 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 Tmem182 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 TMEM182 protein expression.

    This CRISPR knockout system enables efficient generation of Tmem182-deficient cell models for investigation of TMEM182 signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.

    Key Features

    • sgRNAs targeting Tmem182 exon(s) critical for TMEM182 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 Tmem182 genomic sites to improve knockout efficiency
    • Compatible with delivery by transfection

    Design Variants

    CRISPRs +/- HDRs

    • gRNAs encoded by TMEM182 CRISPR/Cas9 KO Plasmid (m) and TMEM182 CRISPR/Cas9 KO Plasmid (m2) target distinct sites within the Tmem182 locus. One or both targeting designs may be available. See Related Products for availability.
    • HDR donor constructs encoded by TMEM182 HDR Plasmid (m) and TMEM182 HDR Plasmid (m2) contain a puromycin resistance cassette and an RFP reporter flanked by Tmem182 homology arms to support homology-directed repair at defined Tmem182 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.