Sclerostin CRISPR/Cas9 KO Plasmid (h): sc-401527
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- Sclerostin 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 Sclerostin 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: Sclerostin Antibody (C-11): sc-518161
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
Sclerostin CRISPR/Cas9 KO Plasmid (h) | sc-401527 | 20 µg | $397.00 |
Overview
SOST encodes sclerostin, a secreted glycoprotein produced primarily by osteocytes that acts as a key negative regulator of bone formation. Sclerostin binds the LRP5/6 co-receptors to antagonize canonical Wnt/β-catenin signaling, thereby modulating osteoblast differentiation, bone matrix deposition, and skeletal remodeling. Through its control of Wnt-driven transcriptional programs, SOST influences osteoblast–osteoclast coupling and mineral homeostasis. Dysregulated SOST activity is associated with altered bone mass phenotypes and is frequently studied in the context of osteoporosis biology, skeletal dysplasias, and bone remodeling changes observed in inflammatory and metabolic disorders.
Sclerostin CRISPR/Cas9 KO Plasmid (h) is a pool of plasmids designed for targeted disruption of the SOST gene in human cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the SOST 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 SOST 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 Sclerostin protein expression.
This CRISPR knockout system enables efficient generation of SOST-deficient cell models for investigation of Sclerostin signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.
Key Features
- sgRNAs targeting SOST exon(s) critical for Sclerostin 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 SOST genomic sites to improve knockout efficiency
- Compatible with delivery by transfection
Design Variants
CRISPRs +/- HDRs
- gRNAs encoded by Sclerostin CRISPR/Cas9 KO Plasmid (h) and Sclerostin CRISPR/Cas9 KO Plasmid (h2) target distinct sites within the SOST locus. One or both targeting designs may be available. See Related Products for availability.
- HDR donor constructs encoded by Sclerostin HDR Plasmid (h) and Sclerostin HDR Plasmid (h2) contain a puromycin resistance cassette and an RFP reporter flanked by SOST homology arms to support homology-directed repair at defined SOST 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.