ARF4 CRISPR/Cas9 KO Plasmid (m): sc-419189
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- ARF4 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 ARF4 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 | |
ARF4 CRISPR/Cas9 KO Plasmid (m) | sc-419189 | 20 µg | $397.00 |
Overview
Arf4 encodes ADP-ribosylation factor 4 (ARF4), a small GTPase of the ARF family that regulates membrane trafficking and lipid remodeling at the Golgi and endosomal system. ARF4 cycles between GDP- and GTP-bound states to coordinate vesicle budding, cargo sorting, and receptor transport, including pathways controlling secretory traffic and ciliary targeting. Through interactions with coat/adaptor machinery and phosphoinositide metabolism, ARF4 helps maintain organelle organization and polarized membrane delivery. Dysregulated ARF4-dependent trafficking has been implicated in altered receptor signaling, ciliogenesis defects, and cellular stress responses relevant to neurobiology, epithelial homeostasis, and tumor-associated phenotypes.
ARF4 CRISPR/Cas9 KO Plasmid (m) is a pool of plasmids designed for targeted disruption of the Arf4 gene in mouse cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the Arf4 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 Arf4 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 ARF4 protein expression.
This CRISPR knockout system enables efficient generation of Arf4-deficient cell models for investigation of ARF4 signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.
Key Features
- sgRNAs targeting Arf4 exon(s) critical for ARF4 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 Arf4 genomic sites to improve knockout efficiency
- Compatible with delivery by transfection
Design Variants
CRISPRs +/- HDRs
- gRNAs encoded by ARF4 CRISPR/Cas9 KO Plasmid (m) and ARF4 CRISPR/Cas9 KO Plasmid (m2) target distinct sites within the Arf4 locus. One or both targeting designs may be available. See Related Products for availability.
- HDR donor constructs encoded by ARF4 HDR Plasmid (m) and ARF4 HDR Plasmid (m2) contain a puromycin resistance cassette and an RFP reporter flanked by Arf4 homology arms to support homology-directed repair at defined Arf4 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.