Myosin VIIB CRISPR/Cas9 KO Plasmid (m): sc-421802
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- Myosin VIIB 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 Myosin VIIB 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 | |
Myosin VIIB CRISPR/Cas9 KO Plasmid (m) | sc-421802 | 20 µg | $397.00 |
Overview
Myo7b encodes myosin VIIB, an actin-based motor protein enriched in polarized epithelial cells where it contributes to cytoskeletal remodeling, apical trafficking, and maintenance of microvillar architecture. Through interactions with actin filaments and membrane-associated complexes, myosin VIIB supports brush border assembly and organization of membrane proteins involved in absorption and barrier function. Disruption of MYO7B-dependent processes is relevant to epithelial dysfunction and altered intestinal homeostasis, making it a useful target for studying polarity, cell junction dynamics, and surface specialization. Mouse Myo7b models help interrogate conserved pathways linking actin motor activity to epithelial morphogenesis and tissue maintenance.
Myosin VIIB CRISPR/Cas9 KO Plasmid (m) is a pool of plasmids designed for targeted disruption of the Myo7b gene in mouse cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the Myo7b 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 Myo7b 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 Myosin VIIB protein expression.
This CRISPR knockout system enables efficient generation of Myo7b-deficient cell models for investigation of Myosin VIIB signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.
Key Features
- sgRNAs targeting Myo7b exon(s) critical for Myosin VIIB 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 Myo7b genomic sites to improve knockout efficiency
- Compatible with delivery by transfection
Design Variants
CRISPRs +/- HDRs
- gRNAs encoded by Myosin VIIB CRISPR/Cas9 KO Plasmid (m) and Myosin VIIB CRISPR/Cas9 KO Plasmid (m2) target distinct sites within the Myo7b locus. One or both targeting designs may be available. See Related Products for availability.
- HDR donor constructs encoded by Myosin VIIB HDR Plasmid (m) and Myosin VIIB HDR Plasmid (m2) contain a puromycin resistance cassette and an RFP reporter flanked by Myo7b homology arms to support homology-directed repair at defined Myo7b 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.