LRP4 CRISPR/Cas9 KO Plasmid (h): sc-401708
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- LRP4 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 LRP4 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 | |
LRP4 CRISPR/Cas9 KO Plasmid (h) | sc-401708 | 20 µg | $397.00 |
Overview
LRP4 (low-density lipoprotein receptor–related protein 4) is a single-pass transmembrane receptor of the LDL receptor family that functions as a co-receptor and signaling scaffold at the cell surface. It is best known for regulating neuromuscular synapse development through agrin–LRP4–MuSK signaling, coordinating acetylcholine receptor clustering and synaptic maturation. LRP4 also modulates Wnt/β-catenin and BMP-related signaling outputs by binding extracellular ligands and influencing pathway availability at the membrane. Genetic and autoimmune perturbations of LRP4 have been associated with neuromuscular junction disorders and skeletal phenotypes, supporting its importance in receptor trafficking, synaptic organization, and tissue patterning.
LRP4 CRISPR/Cas9 KO Plasmid (h) is a pool of plasmids designed for targeted disruption of the LRP4 gene in human cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the LRP4 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 LRP4 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 LRP4 protein expression.
This CRISPR knockout system enables efficient generation of LRP4-deficient cell models for investigation of LRP4 signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.
Key Features
- sgRNAs targeting LRP4 exon(s) critical for LRP4 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 LRP4 genomic sites to improve knockout efficiency
- Compatible with delivery by transfection
Design Variants
CRISPRs +/- HDRs
- gRNAs encoded by LRP4 CRISPR/Cas9 KO Plasmid (h) and LRP4 CRISPR/Cas9 KO Plasmid (h2) target distinct sites within the LRP4 locus. One or both targeting designs may be available. See Related Products for availability.
- HDR donor constructs encoded by LRP4 HDR Plasmid (h) and LRP4 HDR Plasmid (h2) contain a puromycin resistance cassette and an RFP reporter flanked by LRP4 homology arms to support homology-directed repair at defined LRP4 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.