α-actinin-1 CRISPR/Cas9 KO Plasmid (m2): sc-430958-KO-2
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- α-actinin-1 CRISPR/Cas9 Knockout (KO) Plasmid (m2) 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 α-actinin-1 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 | |
α-actinin-1 CRISPR/Cas9 KO Plasmid (m2) | sc-430958-KO-2 | 20 µg | $397.00 |
Overview
Actn1 encodes α-actinin-1, a Ca2+-insensitive actin-binding protein that crosslinks filamentous actin and organizes cortical actin networks, stress fibers, and adhesion-associated cytoskeletal structures. In mouse cells, α-actinin-1 supports integrin-linked focal adhesion dynamics, mechanotransduction, and cell migration by coordinating actin remodeling with signaling hubs such as Rho-family GTPases. Through its role in maintaining cytoskeletal tension and membrane stability, ACTN1 is relevant to studies of platelet biogenesis and hemostatic function, where altered actin architecture can perturb proplatelet formation and cytoskeletal resilience. Dysregulated α-actinin-1 function has been associated with inherited platelet disorders and broader phenotypes involving adhesion and tissue architecture, making Actn1 a useful target for modeling cytoskeleton-driven disease mechanisms.
α-actinin-1 CRISPR/Cas9 KO Plasmid (m2) is a pool of plasmids designed for targeted disruption of the Actn1 gene in mouse cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the Actn1 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 Actn1 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 α-actinin-1 protein expression.
This CRISPR knockout system enables efficient generation of Actn1-deficient cell models for investigation of α-actinin-1 signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.
Key Features
- sgRNAs targeting Actn1 exon(s) critical for α-actinin-1 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 Actn1 genomic sites to improve knockout efficiency
- Compatible with delivery by transfection
Design Variants
CRISPRs +/- HDRs
- gRNAs encoded by α-actinin-1 CRISPR/Cas9 KO Plasmid (m) and α-actinin-1 CRISPR/Cas9 KO Plasmid (m2) target distinct sites within the Actn1 locus. One or both targeting designs may be available. See Related Products for availability.
- HDR donor constructs encoded by α-actinin-1 HDR Plasmid (m) and α-actinin-1 HDR Plasmid (m2) contain a puromycin resistance cassette and an RFP reporter flanked by Actn1 homology arms to support homology-directed repair at defined Actn1 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.