AK1 CRISPR/Cas9 KO Plasmid (m): sc-419062
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- AK1 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 AK1 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: AK1 Antibody (E-8): sc-365316
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
AK1 CRISPR/Cas9 KO Plasmid (m) | sc-419062 | 20 µg | $397.00 |
Overview
Ak1 encodes adenylate kinase 1 (AK1), a cytosolic phosphotransferase that catalyzes the reversible reaction ATP + AMP ⇌ 2 ADP, helping maintain adenine nucleotide homeostasis and buffering cellular energy charge. By coupling ATP/ADP/AMP interconversion to glycolysis and oxidative phosphorylation demand, AK1 influences energetic flux in high-turnover contexts such as muscle contraction, neuronal activity, and stress responses. Altered adenylate kinase activity can modulate AMP-dependent signaling, including pathways that interface with AMPK and purine metabolism, linking Ak1 to metabolic adaptation and redox balance. In mouse systems, perturbing Ak1 supports studies of energy metabolism, mitochondrial function, and phenotypes relevant to cardiometabolic and neuromuscular dysfunction without implying clinical outcomes.
AK1 CRISPR/Cas9 KO Plasmid (m) is a pool of plasmids designed for targeted disruption of the Ak1 gene in mouse cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the Ak1 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 Ak1 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 AK1 protein expression.
This CRISPR knockout system enables efficient generation of Ak1-deficient cell models for investigation of AK1 signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.
Key Features
- sgRNAs targeting Ak1 exon(s) critical for AK1 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 Ak1 genomic sites to improve knockout efficiency
- Compatible with delivery by transfection
Design Variants
CRISPRs +/- HDRs
- gRNAs encoded by AK1 CRISPR/Cas9 KO Plasmid (m) and AK1 CRISPR/Cas9 KO Plasmid (m2) target distinct sites within the Ak1 locus. One or both targeting designs may be available. See Related Products for availability.
- HDR donor constructs encoded by AK1 HDR Plasmid (m) and AK1 HDR Plasmid (m2) contain a puromycin resistance cassette and an RFP reporter flanked by Ak1 homology arms to support homology-directed repair at defined Ak1 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.