fish CRISPR/Cas9 KO Plasmid (h): sc-401277
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- fish 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 fish 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: fish Antibody (G-7): sc-376211
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
fish CRISPR/Cas9 KO Plasmid (h) | sc-401277 | 20 µg | $397.00 |
Overview
SH3PXD2A encodes the adaptor protein TKS5, a Src substrate that scaffolds actin-regulatory and signaling complexes required for podosome and invadopodia formation. Through its SH3 domains and PX domain, TKS5 coordinates PI3K-dependent membrane dynamics, actin polymerization machinery, and metalloprotease trafficking to support extracellular matrix remodeling and cell migration. SH3PXD2A-driven cytoskeletal reorganization is linked to invasive cell behavior and altered tissue architecture, making it relevant to studies of tumor progression, fibrosis-associated remodeling, and vascular cell motility. In immune and stromal contexts, perturbation of TKS5 impacts adhesion structures and directional migration programs that intersect with Src/FAK signaling and Rho-family GTPase pathways.
fish CRISPR/Cas9 KO Plasmid (h) is a pool of plasmids designed for targeted disruption of the SH3PXD2A gene in human cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the SH3PXD2A 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 SH3PXD2A 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 fish protein expression.
This CRISPR knockout system enables efficient generation of SH3PXD2A-deficient cell models for investigation of fish signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.
Key Features
- sgRNAs targeting SH3PXD2A exon(s) critical for fish 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 SH3PXD2A genomic sites to improve knockout efficiency
- Compatible with delivery by transfection
Design Variants
CRISPRs +/- HDRs
- gRNAs encoded by fish CRISPR/Cas9 KO Plasmid (h) and fish CRISPR/Cas9 KO Plasmid (h2) target distinct sites within the SH3PXD2A locus. One or both targeting designs may be available. See Related Products for availability.
- HDR donor constructs encoded by fish HDR Plasmid (h) and fish HDR Plasmid (h2) contain a puromycin resistance cassette and an RFP reporter flanked by SH3PXD2A homology arms to support homology-directed repair at defined SH3PXD2A 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.