ACTA1 CRISPR/Cas9 KO Plasmid (m): sc-418964
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- ACTA1 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 ACTA1 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 | |
ACTA1 CRISPR/Cas9 KO Plasmid (m) | sc-418964 | 20 µg | $397.00 |
Overview
Acta1 encodes ACTA1, the predominant sarcomeric α-actin isoform in skeletal muscle, where it polymerizes into thin filaments that anchor to Z-discs and enable actomyosin-based contraction. ACTA1 integrates structural cytoskeleton organization with calcium-regulated contractile signaling, supporting myofibrillogenesis, sarcomere maintenance, and mechanical force transmission. Altered ACTA1 function perturbs muscle fiber integrity and contractility and is associated with congenital myopathies, making it a central node for studying sarcomere assembly defects and muscle degeneration mechanisms in vivo and in vitro. In mouse systems, Acta1 serves as a key marker and functional determinant for skeletal muscle differentiation, fiber-type remodeling, and stress responses to mechanical load.
ACTA1 CRISPR/Cas9 KO Plasmid (m) is a pool of plasmids designed for targeted disruption of the Acta1 gene in mouse cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the Acta1 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 Acta1 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 ACTA1 protein expression.
This CRISPR knockout system enables efficient generation of Acta1-deficient cell models for investigation of ACTA1 signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.
Key Features
- sgRNAs targeting Acta1 exon(s) critical for ACTA1 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 Acta1 genomic sites to improve knockout efficiency
- Compatible with delivery by transfection
Design Variants
CRISPRs +/- HDRs
- gRNAs encoded by ACTA1 CRISPR/Cas9 KO Plasmid (m) and ACTA1 CRISPR/Cas9 KO Plasmid (m2) target distinct sites within the Acta1 locus. One or both targeting designs may be available. See Related Products for availability.
- HDR donor constructs encoded by ACTA1 HDR Plasmid (m) and ACTA1 HDR Plasmid (m2) contain a puromycin resistance cassette and an RFP reporter flanked by Acta1 homology arms to support homology-directed repair at defined Acta1 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.