ACTL7B CRISPR/Cas9 KO Plasmid (m): sc-418970
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- ACTL7B 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 ACTL7B 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
- Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: ACTL7B Antibody (F-1): sc-398446
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
ACTL7B CRISPR/Cas9 KO Plasmid (m) | sc-418970 | 20 µg | $397.00 |
Overview
Actl7b encodes ACTL7B, a testis-enriched actin-like protein implicated in cytoskeletal remodeling during spermatid differentiation and sperm morphogenesis. As an actin family member, ACTL7B is linked to processes that shape the acrosome–nucleus complex and support organization of microfilament-dependent structures required for motility and fertilization competence. Perturbation of actin dynamics in germ cells is associated with abnormal sperm head formation, reduced sperm function, and male subfertility phenotypes. Actl7b therefore serves as a useful entry point for studying cytoskeletal regulation, spermiogenesis, and gene networks that govern reproductive fitness in mouse models.
ACTL7B CRISPR/Cas9 KO Plasmid (m) is a pool of plasmids designed for targeted disruption of the Actl7b gene in mouse cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the Actl7b 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 Actl7b 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 ACTL7B protein expression.
This CRISPR knockout system enables efficient generation of Actl7b-deficient cell models for investigation of ACTL7B signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.
Key Features
- sgRNAs targeting Actl7b exon(s) critical for ACTL7B 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 Actl7b genomic sites to improve knockout efficiency
- Compatible with delivery by transfection
Design Variants
CRISPRs +/- HDRs
- gRNAs encoded by ACTL7B CRISPR/Cas9 KO Plasmid (m) and ACTL7B CRISPR/Cas9 KO Plasmid (m2) target distinct sites within the Actl7b locus. One or both targeting designs may be available. See Related Products for availability.
- HDR donor constructs encoded by ACTL7B HDR Plasmid (m) and ACTL7B HDR Plasmid (m2) contain a puromycin resistance cassette and an RFP reporter flanked by Actl7b homology arms to support homology-directed repair at defined Actl7b 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.