β-tectorin CRISPR/Cas9 KO Plasmid (m): sc-423332
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- β-tectorin 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 β-tectorin 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 | |
β-tectorin CRISPR/Cas9 KO Plasmid (m) | sc-423332 | 20 µg | $397.00 |
Overview
Tectb encodes β-tectorin, a secreted glycoprotein that contributes to the extracellular matrix architecture of the inner ear tectorial membrane, where it helps organize supramolecular assemblies important for cochlear mechanics. By shaping the biomechanical coupling between the tectorial membrane and hair-cell stereocilia, β-tectorin supports efficient mechanoelectrical transduction and sound-evoked signaling. Disruption of tectorial membrane matrix components, including β-tectorin-associated networks, is linked to altered auditory thresholds and sensorineural hearing phenotypes, making Tectb a useful locus for studying matrix-dependent regulation of sensory function. In mouse models, Tectb perturbation enables analysis of extracellular matrix assembly, epithelial secretion, and structure–function relationships underlying auditory processing.
β-tectorin CRISPR/Cas9 KO Plasmid (m) is a pool of plasmids designed for targeted disruption of the Tectb gene in mouse cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the Tectb 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 Tectb 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 β-tectorin protein expression.
This CRISPR knockout system enables efficient generation of Tectb-deficient cell models for investigation of β-tectorin signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.
Key Features
- sgRNAs targeting Tectb exon(s) critical for β-tectorin 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 Tectb genomic sites to improve knockout efficiency
- Compatible with delivery by transfection
Design Variants
CRISPRs +/- HDRs
- gRNAs encoded by β-tectorin CRISPR/Cas9 KO Plasmid (m) and β-tectorin CRISPR/Cas9 KO Plasmid (m2) target distinct sites within the Tectb locus. One or both targeting designs may be available. See Related Products for availability.
- HDR donor constructs encoded by β-tectorin HDR Plasmid (m) and β-tectorin HDR Plasmid (m2) contain a puromycin resistance cassette and an RFP reporter flanked by Tectb homology arms to support homology-directed repair at defined Tectb 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.