Date published: 2026-8-15

1-800-457-3801

SCBT Portrait Logo
Seach Input

TMEM175 CRISPR/Cas9 KO Plasmid (h): sc-413613

0.0(0)
Write a reviewAsk a question

Datasheets
  • Target species: human
  • 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
  • TMEM175 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 TMEM175 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
    Gene Editing Promo Banner

    Ordering Information

    Product NameCatalog #UNITPriceQtyFAVORITES

    TMEM175 CRISPR/Cas9 KO Plasmid (h)

    sc-413613
    20 µg
    $397.00

    Overview

    TMEM175 encodes a lysosomal and late endosomal transmembrane channel that supports organellar ion homeostasis and lumenal pH stability. By regulating lysosomal function, TMEM175 influences autophagic flux, endolysosomal trafficking, and proteostasis pathways that govern degradation of proteins and damaged organelles. Altered TMEM175 activity has been linked to disrupted lysosome-dependent clearance and cellular stress responses, connecting this gene to neurodegeneration-relevant mechanisms. TMEM175 is therefore studied in the context of lysosome biology, mitochondrial quality control crosstalk, and pathways that modulate inflammatory and metabolic adaptation.

    TMEM175 CRISPR/Cas9 KO Plasmid (h) is a pool of plasmids designed for targeted disruption of the TMEM175 gene in human cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the TMEM175 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 TMEM175 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 TMEM175 protein expression.

    This CRISPR knockout system enables efficient generation of TMEM175-deficient cell models for investigation of TMEM175 signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.

    Key Features

    • sgRNAs targeting TMEM175 exon(s) critical for TMEM175 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 TMEM175 genomic sites to improve knockout efficiency
    • Compatible with delivery by transfection

    Design Variants

    CRISPRs +/- HDRs

    • gRNAs encoded by TMEM175 CRISPR/Cas9 KO Plasmid (h) and TMEM175 CRISPR/Cas9 KO Plasmid (h2) target distinct sites within the TMEM175 locus. One or both targeting designs may be available. See Related Products for availability.
    • HDR donor constructs encoded by TMEM175 HDR Plasmid (h) and TMEM175 HDR Plasmid (h2) contain a puromycin resistance cassette and an RFP reporter flanked by TMEM175 homology arms to support homology-directed repair at defined TMEM175 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.