LRRC50 CRISPR/Cas9 KO Plasmid (h): sc-407107
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- LRRC50 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 LRRC50 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 | |
LRRC50 CRISPR/Cas9 KO Plasmid (h) | sc-407107 | 20 µg | $397.00 |
Overview
DNAAF1 (LRRC50) encodes a leucine-rich repeat protein required for cytoplasmic preassembly of axonemal dynein arms, a key step in motile cilia biogenesis. It supports dynein motor complex maturation and trafficking prior to incorporation into the axoneme, thereby regulating ciliary beating and mucociliary clearance. Disruption of DNAAF1 impairs outer and inner dynein arm formation and compromises cilia-driven fluid flow. Pathogenic variants are linked to primary ciliary dyskinesia with laterality defects, making DNAAF1 a relevant target for studying ciliopathies and cilia-dependent developmental programs.
LRRC50 CRISPR/Cas9 KO Plasmid (h) is a pool of plasmids designed for targeted disruption of the DNAAF1 gene in human cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the DNAAF1 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 DNAAF1 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 LRRC50 protein expression.
This CRISPR knockout system enables efficient generation of DNAAF1-deficient cell models for investigation of LRRC50 signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.
Key Features
- sgRNAs targeting DNAAF1 exon(s) critical for LRRC50 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 DNAAF1 genomic sites to improve knockout efficiency
- Compatible with delivery by transfection
Design Variants
CRISPRs +/- HDRs
- gRNAs encoded by LRRC50 CRISPR/Cas9 KO Plasmid (h) and LRRC50 CRISPR/Cas9 KO Plasmid (h2) target distinct sites within the DNAAF1 locus. One or both targeting designs may be available. See Related Products for availability.
- HDR donor constructs encoded by LRRC50 HDR Plasmid (h) and LRRC50 HDR Plasmid (h2) contain a puromycin resistance cassette and an RFP reporter flanked by DNAAF1 homology arms to support homology-directed repair at defined DNAAF1 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.