Not CRISPR data: the image illustrates antibody quality for visualizing CRISPR experiment results.
Not CRISPR data: the image illustrates antibody quality for visualizing CRISPR experiment results.
ARF6 CRISPR/Cas9 KO Plasmid (m): sc-419191
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- ARF6 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 ARF6 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: ARF6 Antibody (3A-1): sc-7971
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
ARF6 CRISPR/Cas9 KO Plasmid (m) | sc-419191 | 20 µg | $397.00 |
Overview
Arf6 encodes ADP-ribosylation factor 6 (ARF6), a small GTPase that regulates plasma membrane trafficking, endocytosis, and actin cytoskeleton remodeling. ARF6 functions in cycling between GDP- and GTP-bound states to coordinate vesicle recycling, integrin turnover, and membrane ruffle formation, linking signaling inputs to cell shape and motility programs. It interfaces with phosphoinositide metabolism and Rho family GTPase networks to control adhesion dynamics and cortical actin organization. Dysregulated ARF6 signaling has been associated with altered migration and invasion phenotypes and with perturbations in neuronal and immune cell membrane trafficking, supporting its relevance to mechanistic studies of disease-associated cellular behavior.
ARF6 CRISPR/Cas9 KO Plasmid (m) is a pool of plasmids designed for targeted disruption of the Arf6 gene in mouse cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the Arf6 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 Arf6 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 ARF6 protein expression.
This CRISPR knockout system enables efficient generation of Arf6-deficient cell models for investigation of ARF6 signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.
Key Features
- sgRNAs targeting Arf6 exon(s) critical for ARF6 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 Arf6 genomic sites to improve knockout efficiency
- Compatible with delivery by transfection
Design Variants
CRISPRs +/- HDRs
- gRNAs encoded by ARF6 CRISPR/Cas9 KO Plasmid (m) and ARF6 CRISPR/Cas9 KO Plasmid (m2) target distinct sites within the Arf6 locus. One or both targeting designs may be available. See Related Products for availability.
- HDR donor constructs encoded by ARF6 HDR Plasmid (m) and ARF6 HDR Plasmid (m2) contain a puromycin resistance cassette and an RFP reporter flanked by Arf6 homology arms to support homology-directed repair at defined Arf6 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.