TMIE CRISPR/Cas9 KO Plasmid (m): sc-423149
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- TMIE 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 TMIE 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 | |
TMIE CRISPR/Cas9 KO Plasmid (m) | sc-423149 | 20 µg | $397.00 |
Overview
Mouse Tmie encodes TMIE, a small transmembrane protein that functions as an essential component of the mechanotransduction machinery in inner ear hair cells. TMIE participates in assembly and stabilization of the MET channel complex at stereocilia, supporting conversion of mechanical stimuli into receptor potentials that drive auditory signaling. Disruption of TMIE perturbs hair-bundle function, alters ion flux and membrane excitability, and compromises sensory transduction pathways required for hearing and balance. Genetic defects in TMIE/Tmie are linked to hereditary deafness phenotypes, making it a relevant target for studying cochlear development, hair-cell physiology, and sensory-neuron circuit function in mouse models.
TMIE CRISPR/Cas9 KO Plasmid (m) is a pool of plasmids designed for targeted disruption of the Tmie gene in mouse cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the Tmie 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 Tmie 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 TMIE protein expression.
This CRISPR knockout system enables efficient generation of Tmie-deficient cell models for investigation of TMIE signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.
Key Features
- sgRNAs targeting Tmie exon(s) critical for TMIE 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 Tmie genomic sites to improve knockout efficiency
- Compatible with delivery by transfection
Design Variants
CRISPRs +/- HDRs
- gRNAs encoded by TMIE CRISPR/Cas9 KO Plasmid (m) and TMIE CRISPR/Cas9 KO Plasmid (m2) target distinct sites within the Tmie locus. One or both targeting designs may be available. See Related Products for availability.
- HDR donor constructs encoded by TMIE HDR Plasmid (m) and TMIE HDR Plasmid (m2) contain a puromycin resistance cassette and an RFP reporter flanked by Tmie homology arms to support homology-directed repair at defined Tmie 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.