OTOP1 CRISPR/Cas9 KO Plasmid (m): sc-423421
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- OTOP1 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 OTOP1 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
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
OTOP1 CRISPR/Cas9 KO Plasmid (m) | sc-423421 | 20 µg | $397.00 |
Overview
Otop1 encodes OTOP1, a multi-pass membrane protein that functions as a proton-selective ion channel and contributes to cellular pH sensing and regulation. In mouse, OTOP1 activity is linked to vestibular physiology and otoconia biomineralization, processes that depend on tightly controlled ionic microenvironments and calcium carbonate deposition. By modulating proton flux across membranes, OTOP1 can influence acid–base homeostasis and downstream signaling events that are sensitive to extracellular and intracellular pH. Dysregulation of OTOP1-dependent proton handling has been associated with defects in balance and inner ear function, making it a useful target for mechanistic studies of sensory biology.
OTOP1 CRISPR/Cas9 KO Plasmid (m) is a pool of plasmids designed for targeted disruption of the Otop1 gene in mouse cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the Otop1 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 Otop1 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 OTOP1 protein expression.
This CRISPR knockout system enables efficient generation of Otop1-deficient cell models for investigation of OTOP1 signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.
Key Features
- sgRNAs targeting Otop1 exon(s) critical for OTOP1 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 Otop1 genomic sites to improve knockout efficiency
- Compatible with delivery by transfection
Design Variants
CRISPRs +/- HDRs
- gRNAs encoded by OTOP1 CRISPR/Cas9 KO Plasmid (m) and OTOP1 CRISPR/Cas9 KO Plasmid (m2) target distinct sites within the Otop1 locus. One or both targeting designs may be available. See Related Products for availability.
- HDR donor constructs encoded by OTOP1 HDR Plasmid (m) and OTOP1 HDR Plasmid (m2) contain a puromycin resistance cassette and an RFP reporter flanked by Otop1 homology arms to support homology-directed repair at defined Otop1 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.