LRRC26 CRISPR/Cas9 KO Plasmid (m): sc-432708
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- LRRC26 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 LRRC26 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 | |
LRRC26 CRISPR/Cas9 KO Plasmid (m) | sc-432708 | 20 µg | $397.00 |
Overview
Lrrc26 encodes LRRC26, a leucine-rich repeat–containing auxiliary protein that modulates large-conductance Ca2+- and voltage-activated potassium (BK) channel gating. By shifting BK channel activation to more physiological membrane potentials, LRRC26 influences membrane excitability, Ca2+ signaling dynamics, and epithelial ion transport processes. This regulatory role links LRRC26 to pathways controlling smooth muscle tone, secretory epithelial function, and stimulus-secretion coupling. Altered BK channel regulation and auxiliary subunit expression have been associated with physiological dysfunction in excitable and epithelial tissues, supporting the use of Lrrc26 models to interrogate mechanisms relevant to channelopathies and tissue homeostasis.
LRRC26 CRISPR/Cas9 KO Plasmid (m) is a pool of plasmids designed for targeted disruption of the Lrrc26 gene in mouse cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the Lrrc26 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 Lrrc26 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 LRRC26 protein expression.
This CRISPR knockout system enables efficient generation of Lrrc26-deficient cell models for investigation of LRRC26 signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.
Key Features
- sgRNAs targeting Lrrc26 exon(s) critical for LRRC26 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 Lrrc26 genomic sites to improve knockout efficiency
- Compatible with delivery by transfection
Design Variants
CRISPRs +/- HDRs
- gRNAs encoded by LRRC26 CRISPR/Cas9 KO Plasmid (m) and LRRC26 CRISPR/Cas9 KO Plasmid (m2) target distinct sites within the Lrrc26 locus. One or both targeting designs may be available. See Related Products for availability.
- HDR donor constructs encoded by LRRC26 HDR Plasmid (m) and LRRC26 HDR Plasmid (m2) contain a puromycin resistance cassette and an RFP reporter flanked by Lrrc26 homology arms to support homology-directed repair at defined Lrrc26 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.