Acrp30 CRISPR/Cas9 KO Plasmid (m): sc-418962
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- Acrp30 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 Acrp30 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 | |
Acrp30 CRISPR/Cas9 KO Plasmid (m) | sc-418962 | 20 µg | $397.00 |
Overview
Adipoq encodes Acrp30 (adiponectin), an adipocyte-secreted hormone that circulates as multimers and regulates systemic energy balance. Acrp30 signals primarily through ADIPOR1/ADIPOR2 to modulate AMPK and PPARα pathways, influencing fatty acid oxidation, glucose utilization, and mitochondrial biogenesis, and it can shape inflammatory tone via effects on NF-κB-associated signaling. In mouse models, altered Adipoq expression is linked to adipose tissue dysfunction, insulin resistance, hepatic steatosis, and atherosclerosis-related phenotypes. These properties make Adipoq a key node for studying adipokine signaling, metabolic crosstalk between adipose and liver/muscle, and inflammation-metabolism integration.
Acrp30 CRISPR/Cas9 KO Plasmid (m) is a pool of plasmids designed for targeted disruption of the Adipoq gene in mouse cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the Adipoq 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 Adipoq 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 Acrp30 protein expression.
This CRISPR knockout system enables efficient generation of Adipoq-deficient cell models for investigation of Acrp30 signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.
Key Features
- sgRNAs targeting Adipoq exon(s) critical for Acrp30 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 Adipoq genomic sites to improve knockout efficiency
- Compatible with delivery by transfection
Design Variants
CRISPRs +/- HDRs
- gRNAs encoded by Acrp30 CRISPR/Cas9 KO Plasmid (m) and Acrp30 CRISPR/Cas9 KO Plasmid (m2) target distinct sites within the Adipoq locus. One or both targeting designs may be available. See Related Products for availability.
- HDR donor constructs encoded by Acrp30 HDR Plasmid (m) and Acrp30 HDR Plasmid (m2) contain a puromycin resistance cassette and an RFP reporter flanked by Adipoq homology arms to support homology-directed repair at defined Adipoq 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.