Not CRISPR data: the image illustrates antibody quality for visualizing CRISPR experiment results.
Not CRISPR data: the image illustrates antibody quality for visualizing CRISPR experiment results.
ARH CRISPR/Cas9 KO Plasmid (h): sc-406114
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- ARH 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 ARH 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
- Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: ARH Antibody (F-11): sc-514106
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
ARH CRISPR/Cas9 KO Plasmid (h) | sc-406114 | 20 µg | $397.00 |
Overview
LDLRAP1 encodes the adaptor protein ARH, a key component of clathrin-mediated endocytosis that couples the LDL receptor to the AP-2 complex and clathrin coat for internalization at the plasma membrane. ARH recognizes NPXY motifs in LDLR and coordinates cargo selection, vesicle formation, and receptor trafficking through endosomal compartments. This pathway is central to cellular cholesterol uptake and lipoprotein homeostasis, linking LDLRAP1 function to regulation of lipid metabolism networks. Loss-of-function variants in LDLRAP1 are associated with autosomal recessive hypercholesterolemia, making ARH a useful node for dissecting LDLR internalization defects and downstream signaling consequences.
ARH CRISPR/Cas9 KO Plasmid (h) is a pool of plasmids designed for targeted disruption of the LDLRAP1 gene in human cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the LDLRAP1 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 LDLRAP1 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 ARH protein expression.
This CRISPR knockout system enables efficient generation of LDLRAP1-deficient cell models for investigation of ARH signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.
Key Features
- sgRNAs targeting LDLRAP1 exon(s) critical for ARH 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 LDLRAP1 genomic sites to improve knockout efficiency
- Compatible with delivery by transfection
Design Variants
CRISPRs +/- HDRs
- gRNAs encoded by ARH CRISPR/Cas9 KO Plasmid (h) and ARH CRISPR/Cas9 KO Plasmid (h2) target distinct sites within the LDLRAP1 locus. One or both targeting designs may be available. See Related Products for availability.
- HDR donor constructs encoded by ARH HDR Plasmid (h) and ARH HDR Plasmid (h2) contain a puromycin resistance cassette and an RFP reporter flanked by LDLRAP1 homology arms to support homology-directed repair at defined LDLRAP1 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.