OSMR β Double Nickase Plasmid (h): sc-402700-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- OSMR β Double Nickase Plasmid (h) consists of a pair of plasmids each encoding a D10A mutated Cas9 nuclease and a target-specific 20 nt guide RNA (gRNA) designed to knockout gene expression with greater specificity than its CRISPR/Cas9 KO counterpart
- Paired gRNA sequences are offset by approximately 20 bp to allow for specific Cas9-mediated double nicking of the genomic DNA, which mimics a DSB
- One plasmid in the pair contains a puromycin-resistance gene for selection; the other plasmid in the pair contains a GFP marker to visually confirm transfection
- OSMR β Double Nickase Plasmid (h) and OSMR β Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting OSMR. One or both designs may be available
- Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: OSMR β Antibody (D-10): sc-271695
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
OSMR β Double Nickase Plasmid (h) | sc-402700-NIC | 20 µg | $410.00 | |||
OSMR β Double Nickase Plasmid (h2) | sc-402700-NIC-2 | 20 µg | $410.00 |
Oncostatin M receptor beta (OSMRβ), encoded by the human OSMR gene, is a type I cytokine receptor subunit that forms signaling complexes with GP130 to mediate responses to oncostatin M and related IL-6 family cytokines. Ligand engagement activates JAK/STAT, MAPK/ERK, and PI3K/AKT pathways, linking OSMRβ to transcriptional programs controlling inflammation, extracellular matrix remodeling, and cell-state transitions. OSMR signaling has been implicated in fibrotic and inflammatory biology and in tumor microenvironment-associated processes, where altered pathway activity can influence stromal interactions and invasive phenotypes. As a result, OSMRβ is frequently investigated in studies of cytokine-driven gene regulation, epithelial–mesenchymal plasticity, and immune–stromal crosstalk.
OSMR β Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the OSMR locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within OSMR. 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 OSMR 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 OSMR-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.