Myosin IXa CRISPR/Cas9 KO Plasmid (h): sc-407473
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- Myosin IXa CRISPR/Cas9 Knockout (KO) Plasmid (h) 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 IXa 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 IXa CRISPR/Cas9 KO Plasmid (h) | sc-407473 | 20 µg | $397.00 |
Overview
MYO9A encodes myosin IXa, an unconventional actin-based motor protein that also contains a Rho GTPase-activating (RhoGAP) domain, linking cytoskeletal dynamics to small GTPase signaling. Through regulation of actin remodeling, membrane protrusion, and cell adhesion, myosin IXa contributes to cell polarity and directed migration and can influence RhoA-dependent pathways controlling contractility and junctional organization. These functions position MYO9A as a mechanistic node in processes such as epithelial morphogenesis, neurite outgrowth, and intracellular trafficking where coordinated motor activity and Rho signaling are required. Dysregulation of cytoskeletal control and Rho pathway signaling is implicated across diverse human pathologies, making MYO9A a relevant target for studying disease-associated changes in motility, barrier function, and morphodynamic signaling.
Myosin IXa CRISPR/Cas9 KO Plasmid (h) is a pool of plasmids designed for targeted disruption of the MYO9A gene in human cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the MYO9A 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 MYO9A 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 IXa protein expression.
This CRISPR knockout system enables efficient generation of MYO9A-deficient cell models for investigation of Myosin IXa signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.
Key Features
- sgRNAs targeting MYO9A exon(s) critical for Myosin IXa 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 MYO9A genomic sites to improve knockout efficiency
- Compatible with delivery by transfection
Design Variants
CRISPRs +/- HDRs
- gRNAs encoded by Myosin IXa CRISPR/Cas9 KO Plasmid (h) and Myosin IXa CRISPR/Cas9 KO Plasmid (h2) target distinct sites within the MYO9A locus. One or both targeting designs may be available. See Related Products for availability.
- HDR donor constructs encoded by Myosin IXa HDR Plasmid (h) and Myosin IXa HDR Plasmid (h2) contain a puromycin resistance cassette and an RFP reporter flanked by MYO9A homology arms to support homology-directed repair at defined MYO9A 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.