ACTL7A CRISPR/Cas9 KO Plasmid (m): sc-418969
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- ACTL7A 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 ACTL7A 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 | |
ACTL7A CRISPR/Cas9 KO Plasmid (m) | sc-418969 | 20 µg | $397.00 |
Overview
Actl7a encodes ACTL7A, an actin-like protein with enriched expression in the male germline that contributes to cytoskeletal remodeling during spermatid differentiation. ACTL7A is linked to actin-based processes that shape spermatid head architecture, acrosome formation, and assembly of the perinuclear cytoskeleton, coordinating structural changes required for sperm maturation. Disruption of these cytoskeletal programs can impair spermiogenesis, reduce sperm function, and contribute to male infertility phenotypes in model systems. As a testis-biased actin family member, Actl7a is commonly studied in pathways governing germ cell development and reproductive fitness.
ACTL7A CRISPR/Cas9 KO Plasmid (m) is a pool of plasmids designed for targeted disruption of the Actl7a gene in mouse cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the Actl7a 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 Actl7a 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 ACTL7A protein expression.
This CRISPR knockout system enables efficient generation of Actl7a-deficient cell models for investigation of ACTL7A signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.
Key Features
- sgRNAs targeting Actl7a exon(s) critical for ACTL7A 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 Actl7a genomic sites to improve knockout efficiency
- Compatible with delivery by transfection
Design Variants
CRISPRs +/- HDRs
- gRNAs encoded by ACTL7A CRISPR/Cas9 KO Plasmid (m) and ACTL7A CRISPR/Cas9 KO Plasmid (m2) target distinct sites within the Actl7a locus. One or both targeting designs may be available. See Related Products for availability.
- HDR donor constructs encoded by ACTL7A HDR Plasmid (m) and ACTL7A HDR Plasmid (m2) contain a puromycin resistance cassette and an RFP reporter flanked by Actl7a homology arms to support homology-directed repair at defined Actl7a 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.