β ig-h3 CRISPR/Cas9 KO Plasmid (h): sc-403770
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- β ig-h3 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 β ig-h3 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 | |
β ig-h3 CRISPR/Cas9 KO Plasmid (h) | sc-403770 | 20 µg | $397.00 |
Overview
TGFBI encodes β ig-h3 (TGFBIp), an extracellular matrix protein induced by TGF-β signaling that binds collagens, fibronectin, and integrins to regulate cell adhesion, migration, and matrix organization. Through roles in ECM remodeling and integrin-mediated signaling, β ig-h3 influences epithelial–mesenchymal transition, wound repair, and tissue homeostasis. Altered TGFBI expression has been linked to fibrotic processes and tumor–stroma interactions affecting invasion and metastatic potential. Pathogenic variants and dysregulated deposition of β ig-h3 are also associated with corneal stromal dystrophies and aberrant protein aggregation in ocular tissues.
β ig-h3 CRISPR/Cas9 KO Plasmid (h) is a pool of plasmids designed for targeted disruption of the TGFBI gene in human cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the TGFBI 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 TGFBI 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 β ig-h3 protein expression.
This CRISPR knockout system enables efficient generation of TGFBI-deficient cell models for investigation of β ig-h3 signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.
Key Features
- sgRNAs targeting TGFBI exon(s) critical for β ig-h3 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 TGFBI genomic sites to improve knockout efficiency
- Compatible with delivery by transfection
Design Variants
CRISPRs +/- HDRs
- gRNAs encoded by β ig-h3 CRISPR/Cas9 KO Plasmid (h) and β ig-h3 CRISPR/Cas9 KO Plasmid (h2) target distinct sites within the TGFBI locus. One or both targeting designs may be available. See Related Products for availability.
- HDR donor constructs encoded by β ig-h3 HDR Plasmid (h) and β ig-h3 HDR Plasmid (h2) contain a puromycin resistance cassette and an RFP reporter flanked by TGFBI homology arms to support homology-directed repair at defined TGFBI 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.