



Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
Sclerostin Double Nickase Plasmid (h) | sc-401527-NIC | 20 µg | $410.00 | |||
Sclerostin Double Nickase Plasmid (h2) | sc-401527-NIC-2 | 20 µg | $410.00 |
SOST encodes sclerostin, a secreted glycoprotein predominantly produced by osteocytes that acts as a key extracellular inhibitor of canonical Wnt/β-catenin signaling by binding LRP5/6 co-receptors and limiting osteoblast differentiation and activity. Through modulation of Wnt signaling and cross-talk with BMP pathways, sclerostin helps regulate bone formation, remodeling, and mechanotransduction-dependent responses in skeletal tissue. Altered SOST expression or function is linked to abnormal bone mass phenotypes and is frequently studied in the context of osteoporosis-related pathways, bone density regulation, and skeletal development. In addition to skeletal biology, sclerostin-mediated Wnt regulation is relevant to broader cell fate and extracellular signaling studies where Wnt pathway tone influences proliferation and differentiation programs.
Sclerostin Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the SOST locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within SOST. When directed to adjacent sites on opposite DNA strands, the two nickases generate offset single-strand nicks that together produce a staggered double-strand break, requiring coordinated on-target activity from both guides. The resulting DNA break is resolved by endogenous cellular repair pathways, most commonly through non-homologous end joining (NHEJ), leading to insertions or deletions that disrupt SOST function. By requiring dual sgRNA engagement at the target locus, the double nicking approach enhances editing specificity and provides a complementary CRISPR strategy for applications where additional control over targeting precision is desired.
To support efficient identification of edited cells, one plasmid encodes GFP for fluorescent visualization of transfected populations, while the companion plasmid carries a puromycin resistance gene for antibiotic selection. Together, these features support efficient enrichment of co-transfected populations and simplify the validation of SOST-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.