ACP2 CRISPR/Cas9 KO Plasmid (m): sc-418950
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- ACP2 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 ACP2 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 | |
ACP2 CRISPR/Cas9 KO Plasmid (m) | sc-418950 | 20 µg | $397.00 |
Overview
Acp2 encodes lysosomal acid phosphatase 2 (ACP2), a hydrolase that contributes to phosphate ester turnover within the acidic lumen of lysosomes. ACP2 activity supports lysosome-dependent macromolecule degradation and intersects with endolysosomal trafficking, autophagy, and cellular nutrient recycling pathways. Altered lysosomal phosphatase function can perturb organelle homeostasis and has relevance to mechanisms studied in lysosomal dysfunction and neurodegeneration-related phenotypes. In mouse models, Acp2 is useful for probing how lysosomal enzyme balance influences cellular stress responses, immune cell function, and tissue homeostasis.
ACP2 CRISPR/Cas9 KO Plasmid (m) is a pool of plasmids designed for targeted disruption of the Acp2 gene in mouse cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the Acp2 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 Acp2 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 ACP2 protein expression.
This CRISPR knockout system enables efficient generation of Acp2-deficient cell models for investigation of ACP2 signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.
Key Features
- sgRNAs targeting Acp2 exon(s) critical for ACP2 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 Acp2 genomic sites to improve knockout efficiency
- Compatible with delivery by transfection
Design Variants
CRISPRs +/- HDRs
- gRNAs encoded by ACP2 CRISPR/Cas9 KO Plasmid (m) and ACP2 CRISPR/Cas9 KO Plasmid (m2) target distinct sites within the Acp2 locus. One or both targeting designs may be available. See Related Products for availability.
- HDR donor constructs encoded by ACP2 HDR Plasmid (m) and ACP2 HDR Plasmid (m2) contain a puromycin resistance cassette and an RFP reporter flanked by Acp2 homology arms to support homology-directed repair at defined Acp2 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.