APRT CRISPR/Cas9 KO Plasmid (h): sc-410689
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- APRT 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 APRT 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 | |
APRT CRISPR/Cas9 KO Plasmid (h) | sc-410689 | 20 µg | $397.00 |
Overview
APRT (adenine phosphoribosyltransferase) is a cytosolic phosphoribosyltransferase that catalyzes adenine salvage to adenosine monophosphate using phosphoribosyl pyrophosphate, supporting nucleotide homeostasis and purine metabolism. This activity links the purine salvage pathway with broader cellular processes including DNA/RNA synthesis, energy balance, and replication stress responses that depend on adequate nucleotide pools. Altered APRT function perturbs purine flux and can shift reliance toward de novo purine biosynthesis, providing a tractable system for studying metabolic compensation and nucleotide imbalance. APRT deficiency has been associated with disturbances in purine handling and related renal pathology, making APRT a useful model for interrogating metabolism-linked cellular phenotypes.
APRT CRISPR/Cas9 KO Plasmid (h) is a pool of plasmids designed for targeted disruption of the APRT gene in human cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the APRT 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 APRT 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 APRT protein expression.
This CRISPR knockout system enables efficient generation of APRT-deficient cell models for investigation of APRT signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.
Key Features
- sgRNAs targeting APRT exon(s) critical for APRT 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 APRT genomic sites to improve knockout efficiency
- Compatible with delivery by transfection
Design Variants
CRISPRs +/- HDRs
- gRNAs encoded by APRT CRISPR/Cas9 KO Plasmid (h) and APRT CRISPR/Cas9 KO Plasmid (h2) target distinct sites within the APRT locus. One or both targeting designs may be available. See Related Products for availability.
- HDR donor constructs encoded by APRT HDR Plasmid (h) and APRT HDR Plasmid (h2) contain a puromycin resistance cassette and an RFP reporter flanked by APRT homology arms to support homology-directed repair at defined APRT 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.