AMPD3 CRISPR/Cas9 KO Plasmid (m): sc-419101
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- AMPD3 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 AMPD3 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 | |
AMPD3 CRISPR/Cas9 KO Plasmid (m) | sc-419101 | 20 µg | $397.00 |
Overview
Ampd3 encodes AMP deaminase 3 (AMPD3), an enzyme that catalyzes deamination of AMP to IMP, helping regulate adenine nucleotide balance and cellular energy charge. By modulating AMP availability, AMPD3 influences purine nucleotide metabolism and links energetic stress sensing to downstream metabolic adaptation in tissues with dynamic ATP turnover. Altered AMP deamination can shift IMP/AMP pools and impact pathways connected to nucleotide salvage, mitochondrial function, and redox homeostasis. Dysregulation of purine metabolism is relevant to models of metabolic stress and tissue remodeling, making Ampd3 a useful target for mechanistic studies in mouse systems.
AMPD3 CRISPR/Cas9 KO Plasmid (m) is a pool of plasmids designed for targeted disruption of the Ampd3 gene in mouse cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the Ampd3 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 Ampd3 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 AMPD3 protein expression.
This CRISPR knockout system enables efficient generation of Ampd3-deficient cell models for investigation of AMPD3 signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.
Key Features
- sgRNAs targeting Ampd3 exon(s) critical for AMPD3 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 Ampd3 genomic sites to improve knockout efficiency
- Compatible with delivery by transfection
Design Variants
CRISPRs +/- HDRs
- gRNAs encoded by AMPD3 CRISPR/Cas9 KO Plasmid (m) and AMPD3 CRISPR/Cas9 KO Plasmid (m2) target distinct sites within the Ampd3 locus. One or both targeting designs may be available. See Related Products for availability.
- HDR donor constructs encoded by AMPD3 HDR Plasmid (m) and AMPD3 HDR Plasmid (m2) contain a puromycin resistance cassette and an RFP reporter flanked by Ampd3 homology arms to support homology-directed repair at defined Ampd3 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.