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.
ARL4D CRISPR/Cas9 KO Plasmid (h): sc-406905
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- ARL4D 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 ARL4D 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: ARL4D Antibody (F-2): sc-271273
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
ARL4D CRISPR/Cas9 KO Plasmid (h) | sc-406905 | 20 µg | $397.00 |
Overview
ARL4D (ADP ribosylation factor like GTPase 4D) is a small ARF-like GTP-binding protein that cycles between GDP- and GTP-bound states to coordinate membrane trafficking and cytoskeletal remodeling. It has been implicated in regulation of actin dynamics, vesicular transport, and compartmentalized signaling at cellular membranes, processes that influence cell shape, polarity, and motility. ARL4D activity intersects with small GTPase-controlled pathways that govern membrane recruitment of effectors and organization of trafficking routes. Altered ARL4D expression or signaling has been explored in the context of dysregulated proliferation and migration phenotypes relevant to oncology and other disorders involving membrane dynamics.
ARL4D CRISPR/Cas9 KO Plasmid (h) is a pool of plasmids designed for targeted disruption of the ARL4D gene in human cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the ARL4D 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 ARL4D 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 ARL4D protein expression.
This CRISPR knockout system enables efficient generation of ARL4D-deficient cell models for investigation of ARL4D signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.
Key Features
- sgRNAs targeting ARL4D exon(s) critical for ARL4D 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 ARL4D genomic sites to improve knockout efficiency
- Compatible with delivery by transfection
Design Variants
CRISPRs +/- HDRs
- gRNAs encoded by ARL4D CRISPR/Cas9 KO Plasmid (h) and ARL4D CRISPR/Cas9 KO Plasmid (h2) target distinct sites within the ARL4D locus. One or both targeting designs may be available. See Related Products for availability.
- HDR donor constructs encoded by ARL4D HDR Plasmid (h) and ARL4D HDR Plasmid (h2) contain a puromycin resistance cassette and an RFP reporter flanked by ARL4D homology arms to support homology-directed repair at defined ARL4D 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.