PTH CRISPR/Cas9 KO Plasmid (m): sc-422490
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- PTH 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 PTH 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 | |
PTH CRISPR/Cas9 KO Plasmid (m) | sc-422490 | 20 µg | $397.00 |
Overview
Mouse Pth encodes parathyroid hormone (PTH), a secreted peptide that maintains systemic calcium and phosphate balance by signaling through the PTH1 receptor to regulate bone remodeling, renal tubular reabsorption, and phosphate excretion. PTH-driven GPCR signaling engages cAMP/PKA and PLC/PKC pathways and influences osteoblast–osteoclast coupling via downstream mediators such as RANKL and OPG. In physiological contexts, Pth expression integrates feedback from circulating calcium and vitamin D metabolism to coordinate mineral ion homeostasis. Dysregulated PTH signaling is broadly relevant to research on skeletal turnover, mineral metabolism disorders, and endocrine regulation of kidney–bone axis crosstalk.
PTH CRISPR/Cas9 KO Plasmid (m) is a pool of plasmids designed for targeted disruption of the Pth gene in mouse cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the Pth 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 Pth 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 PTH protein expression.
This CRISPR knockout system enables efficient generation of Pth-deficient cell models for investigation of PTH signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.
Key Features
- sgRNAs targeting Pth exon(s) critical for PTH 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 Pth genomic sites to improve knockout efficiency
- Compatible with delivery by transfection
Design Variants
CRISPRs +/- HDRs
- gRNAs encoded by PTH CRISPR/Cas9 KO Plasmid (m) and PTH CRISPR/Cas9 KO Plasmid (m2) target distinct sites within the Pth locus. One or both targeting designs may be available. See Related Products for availability.
- HDR donor constructs encoded by PTH HDR Plasmid (m) and PTH HDR Plasmid (m2) contain a puromycin resistance cassette and an RFP reporter flanked by Pth homology arms to support homology-directed repair at defined Pth 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.