APEG1 CRISPR/Cas9 KO Plasmid (m): sc-419147
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- APEG1 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 APEG1 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 | |
APEG1 CRISPR/Cas9 KO Plasmid (m) | sc-419147 | 20 µg | $397.00 |
Overview
Speg encodes APEG1, a striated muscle–enriched serine/threonine protein kinase implicated in cytoskeletal organization and excitation–contraction coupling. APEG1 is associated with myofibril integrity and triad/junctional membrane homeostasis, linking kinase signaling to sarcomere assembly and calcium handling processes in cardiomyocytes and skeletal muscle fibers. Disruption of Speg-dependent pathways has been connected to defects in muscle development and contractile function, making it relevant for studying mechanisms underlying cardiomyopathy and myopathy phenotypes in mouse models.
APEG1 CRISPR/Cas9 KO Plasmid (m) is a pool of plasmids designed for targeted disruption of the Speg gene in mouse cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the Speg 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 Speg 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 APEG1 protein expression.
This CRISPR knockout system enables efficient generation of Speg-deficient cell models for investigation of APEG1 signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.
Key Features
- sgRNAs targeting Speg exon(s) critical for APEG1 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 Speg genomic sites to improve knockout efficiency
- Compatible with delivery by transfection
Design Variants
CRISPRs +/- HDRs
- gRNAs encoded by APEG1 CRISPR/Cas9 KO Plasmid (m) and APEG1 CRISPR/Cas9 KO Plasmid (m2) target distinct sites within the Speg locus. One or both targeting designs may be available. See Related Products for availability.
- HDR donor constructs encoded by APEG1 HDR Plasmid (m) and APEG1 HDR Plasmid (m2) contain a puromycin resistance cassette and an RFP reporter flanked by Speg homology arms to support homology-directed repair at defined Speg 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.