Date published: 2026-9-9

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TMEM132C CRISPR/Cas9 KO Plasmid (m): sc-431553

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Datasheets
  • Target species: mouse
  • 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
  • TMEM132C 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 TMEM132C 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

    TMEM132C CRISPR/Cas9 KO Plasmid (m)

    sc-431553
    20 µg
    $397.00

    Overview

    Tmem132c encodes TMEM132C, a predicted multi-pass transmembrane protein that localizes to cellular membranes and is thought to contribute to cell-surface organization and membrane-associated signaling. Members of the TMEM132 family have been linked to regulation of cell adhesion and cytoskeletal dynamics, suggesting roles in tissue architecture and neuronal or epithelial homeostasis. In mouse systems, Tmem132c expression patterns support investigation of how membrane proteins modulate cellular connectivity and stress responses in development and adult physiology. Dysregulation of transmembrane adhesion/signaling modules is commonly explored in studies of neurobiology and complex disease genetics, making TMEM132C a useful target for mechanistic pathway interrogation.

    TMEM132C CRISPR/Cas9 KO Plasmid (m) is a pool of plasmids designed for targeted disruption of the Tmem132c gene in mouse cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the Tmem132c 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 Tmem132c 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 TMEM132C protein expression.

    This CRISPR knockout system enables efficient generation of Tmem132c-deficient cell models for investigation of TMEM132C signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.

    Key Features

    • sgRNAs targeting Tmem132c exon(s) critical for TMEM132C 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 Tmem132c genomic sites to improve knockout efficiency
    • Compatible with delivery by transfection

    Design Variants

    CRISPRs +/- HDRs

    • gRNAs encoded by TMEM132C CRISPR/Cas9 KO Plasmid (m) and TMEM132C CRISPR/Cas9 KO Plasmid (m2) target distinct sites within the Tmem132c locus. One or both targeting designs may be available. See Related Products for availability.
    • HDR donor constructs encoded by TMEM132C HDR Plasmid (m) and TMEM132C HDR Plasmid (m2) contain a puromycin resistance cassette and an RFP reporter flanked by Tmem132c homology arms to support homology-directed repair at defined Tmem132c 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.