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.
AIP2 CRISPR/Cas9 KO Plasmid (h): sc-417914
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- AIP2 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 AIP2 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: AIP2 Antibody (A-3): sc-398090
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
AIP2 CRISPR/Cas9 KO Plasmid (h) | sc-417914 | 20 µg | $397.00 |
Overview
WWP2 encodes the E3 ubiquitin-protein ligase AIP2, a HECT-domain ubiquitin ligase that catalyzes ubiquitin transfer to regulate protein stability and signaling output. AIP2 participates in ubiquitin-dependent control of key cellular processes including proteostasis, receptor and transcription factor turnover, and pathway tuning in contexts such as TGF-β/SMAD signaling and related regulatory networks. Through these functions, WWP2 contributes to modulation of cell growth, differentiation, and epithelial–mesenchymal transition programs. Dysregulated ubiquitination involving WWP2 has been associated with altered signaling states observed in multiple disease-relevant models, supporting its use as a mechanistic node in studies of pathway imbalance.
AIP2 CRISPR/Cas9 KO Plasmid (h) is a pool of plasmids designed for targeted disruption of the WWP2 gene in human cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the WWP2 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 WWP2 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 AIP2 protein expression.
This CRISPR knockout system enables efficient generation of WWP2-deficient cell models for investigation of AIP2 signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.
Key Features
- sgRNAs targeting WWP2 exon(s) critical for AIP2 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 WWP2 genomic sites to improve knockout efficiency
- Compatible with delivery by transfection
Design Variants
CRISPRs +/- HDRs
- gRNAs encoded by AIP2 CRISPR/Cas9 KO Plasmid (h) and AIP2 CRISPR/Cas9 KO Plasmid (h2) target distinct sites within the WWP2 locus. One or both targeting designs may be available. See Related Products for availability.
- HDR donor constructs encoded by AIP2 HDR Plasmid (h) and AIP2 HDR Plasmid (h2) contain a puromycin resistance cassette and an RFP reporter flanked by WWP2 homology arms to support homology-directed repair at defined WWP2 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.