CIP4 CRISPR/Cas9 KO Plasmid (h): sc-406095
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- CIP4 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 CIP4 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: CIP4 Antibody (F-10): sc-166810
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
CIP4 CRISPR/Cas9 KO Plasmid (h) | sc-406095 | 20 µg | $397.00 |
Overview
TRIP10 encodes Cdc42-interacting protein 4 (CIP4), an F-BAR/SH3 domain adaptor that links membrane curvature sensing to actin cytoskeleton remodeling. CIP4 cooperates with Cdc42, dynamin, and N-WASP to coordinate clathrin-mediated endocytosis, vesicle trafficking, and cortical actin assembly, thereby influencing receptor internalization and signal attenuation. Through these functions, CIP4 contributes to processes such as cell polarity, migration, and invadopodia-like protrusion dynamics, connecting it to pathways that regulate cytoskeletal organization and membrane remodeling. Dysregulated TRIP10/CIP4 activity has been studied in the context of aberrant cell motility and signaling programs relevant to cancer biology and other disorders involving altered endocytic and actin networks.
CIP4 CRISPR/Cas9 KO Plasmid (h) is a pool of plasmids designed for targeted disruption of the TRIP10 gene in human cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the TRIP10 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 TRIP10 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 CIP4 protein expression.
This CRISPR knockout system enables efficient generation of TRIP10-deficient cell models for investigation of CIP4 signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.
Key Features
- sgRNAs targeting TRIP10 exon(s) critical for CIP4 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 TRIP10 genomic sites to improve knockout efficiency
- Compatible with delivery by transfection
Design Variants
CRISPRs +/- HDRs
- gRNAs encoded by CIP4 CRISPR/Cas9 KO Plasmid (h) and CIP4 CRISPR/Cas9 KO Plasmid (h2) target distinct sites within the TRIP10 locus. One or both targeting designs may be available. See Related Products for availability.
- HDR donor constructs encoded by CIP4 HDR Plasmid (h) and CIP4 HDR Plasmid (h2) contain a puromycin resistance cassette and an RFP reporter flanked by TRIP10 homology arms to support homology-directed repair at defined TRIP10 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.