ACTC1 CRISPR/Cas9 KO Plasmid (m): sc-418966
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- ACTC1 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 ACTC1 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 | |
ACTC1 CRISPR/Cas9 KO Plasmid (m) | sc-418966 | 20 µg | $397.00 |
Overview
Actc1 encodes alpha cardiac actin (ACTC1), a principal sarcomeric thin-filament component that polymerizes into F-actin and supports force generation in striated muscle. ACTC1 coordinates with myosin, tropomyosin, and the troponin complex to regulate Ca2+-dependent contraction, contributing to myofibril assembly, sarcomere organization, and cytoskeletal mechanotransduction. In mouse, Actc1 is highly relevant to cardiac and skeletal muscle development and remodeling, linking actin filament dynamics to pathways governing contractility, cell structure, and stress responses. Genetic and functional perturbation of ACTC1 is associated with cardiomyopathy-related phenotypes and abnormal muscle function, making it a useful node for studying disease-relevant changes in sarcomere integrity and cardiac physiology.
ACTC1 CRISPR/Cas9 KO Plasmid (m) is a pool of plasmids designed for targeted disruption of the Actc1 gene in mouse cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the Actc1 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 Actc1 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 ACTC1 protein expression.
This CRISPR knockout system enables efficient generation of Actc1-deficient cell models for investigation of ACTC1 signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.
Key Features
- sgRNAs targeting Actc1 exon(s) critical for ACTC1 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 Actc1 genomic sites to improve knockout efficiency
- Compatible with delivery by transfection
Design Variants
CRISPRs +/- HDRs
- gRNAs encoded by ACTC1 CRISPR/Cas9 KO Plasmid (m) and ACTC1 CRISPR/Cas9 KO Plasmid (m2) target distinct sites within the Actc1 locus. One or both targeting designs may be available. See Related Products for availability.
- HDR donor constructs encoded by ACTC1 HDR Plasmid (m) and ACTC1 HDR Plasmid (m2) contain a puromycin resistance cassette and an RFP reporter flanked by Actc1 homology arms to support homology-directed repair at defined Actc1 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.