Noggin Double Nickase Plasmid (h): sc-402090-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- Noggin 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
- Noggin Double Nickase Plasmid (h) and Noggin Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting NOG. One or both designs may be available
- Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: Noggin Antibody (2C10): sc-293439
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
Noggin Double Nickase Plasmid (h) | sc-402090-NIC | 20 µg | $410.00 |
NOG encodes noggin, a secreted antagonist of bone morphogenetic proteins (BMPs) that shapes embryonic patterning and regulates osteogenic and neuroectodermal differentiation by limiting BMP receptor–SMAD1/5/8 signaling. By binding BMP2, BMP4, and related ligands in the extracellular space, noggin modulates gradients that control cell fate decisions, tissue morphogenesis, and skeletal homeostasis. Disruption of NOG-dependent BMP restraint has been associated with congenital skeletal malformations and craniofacial development defects, and altered BMP pathway balance is frequently studied in contexts of fibrosis and tumor microenvironment remodeling. As a pathway node, NOG is widely used to interrogate BMP/TGF-β crosstalk and differentiation programs in human stem and progenitor cell models.
Noggin Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the NOG locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within NOG. 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 NOG 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 NOG-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.