FGF-23 CRISPR/Cas9 KO Plasmid (m): sc-425719
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- FGF-23 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 FGF-23 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 | |
FGF-23 CRISPR/Cas9 KO Plasmid (m) | sc-425719 | 20 µg | $397.00 |
Overview
Fibroblast growth factor 23 (FGF-23), encoded by the mouse Fgf23 gene, is an endocrine FGF predominantly produced by osteocytes and osteoblasts that maintains systemic phosphate and vitamin D balance. Acting through FGFRs in a Klotho-dependent manner, FGF-23 suppresses renal phosphate reabsorption and modulates vitamin D metabolism, thereby coordinating mineral ion homeostasis with bone remodeling. Dysregulated FGF-23 signaling is linked to altered phosphate handling, skeletal mineralization defects, and secondary changes in parathyroid hormone and vitamin D pathways, making it a key node in bone–kidney endocrine crosstalk. As a biomarker-associated regulator of mineral metabolism, Fgf23 is widely studied in models of disordered phosphate homeostasis and related bone and renal physiology.
FGF-23 CRISPR/Cas9 KO Plasmid (m) is a pool of plasmids designed for targeted disruption of the Fgf23 gene in mouse cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the Fgf23 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 Fgf23 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 FGF-23 protein expression.
This CRISPR knockout system enables efficient generation of Fgf23-deficient cell models for investigation of FGF-23 signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.
Key Features
- sgRNAs targeting Fgf23 exon(s) critical for FGF-23 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 Fgf23 genomic sites to improve knockout efficiency
- Compatible with delivery by transfection
Design Variants
CRISPRs +/- HDRs
- gRNAs encoded by FGF-23 CRISPR/Cas9 KO Plasmid (m) and FGF-23 CRISPR/Cas9 KO Plasmid (m2) target distinct sites within the Fgf23 locus. One or both targeting designs may be available. See Related Products for availability.
- HDR donor constructs encoded by FGF-23 HDR Plasmid (m) and FGF-23 HDR Plasmid (m2) contain a puromycin resistance cassette and an RFP reporter flanked by Fgf23 homology arms to support homology-directed repair at defined Fgf23 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.