JWA CRISPR/Cas9 KO Plasmid (h): sc-406231
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- JWA 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 JWA 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 | |
JWA CRISPR/Cas9 KO Plasmid (h) | sc-406231 | 20 µg | $397.00 |
Overview
ARL6IP5 encodes JWA, a stress-responsive membrane-associated protein implicated in regulating cytoskeletal organization, cell adhesion, and vesicular trafficking. JWA has been linked to modulation of MAPK signaling and oxidative stress responses, influencing processes such as migration, proliferation, and apoptosis. In human cells, altered JWA expression has been associated with dysregulated inflammatory signaling and tumor biology, making it relevant for mechanistic studies of cancer progression, metastasis-related phenotypes, and cellular stress adaptation.
JWA CRISPR/Cas9 KO Plasmid (h) is a pool of plasmids designed for targeted disruption of the ARL6IP5 gene in human cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the ARL6IP5 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 ARL6IP5 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 JWA protein expression.
This CRISPR knockout system enables efficient generation of ARL6IP5-deficient cell models for investigation of JWA signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.
Key Features
- sgRNAs targeting ARL6IP5 exon(s) critical for JWA 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 ARL6IP5 genomic sites to improve knockout efficiency
- Compatible with delivery by transfection
Design Variants
CRISPRs +/- HDRs
- gRNAs encoded by JWA CRISPR/Cas9 KO Plasmid (h) and JWA CRISPR/Cas9 KO Plasmid (h2) target distinct sites within the ARL6IP5 locus. One or both targeting designs may be available. See Related Products for availability.
- HDR donor constructs encoded by JWA HDR Plasmid (h) and JWA HDR Plasmid (h2) contain a puromycin resistance cassette and an RFP reporter flanked by ARL6IP5 homology arms to support homology-directed repair at defined ARL6IP5 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.