BMPR-IA Double Nickase Plasmid (m): sc-419350-NIC
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- BMPR-IA Double Nickase Plasmid (m) 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
- BMPR-IA Double Nickase Plasmid (m) and BMPR-IA Double Nickase Plasmid (m2) encode distinct paired gRNA designs targeting Bmpr1a. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
BMPR-IA Double Nickase Plasmid (m) | sc-419350-NIC | 20 µg | $410.00 |
Bmpr1a encodes BMPR-IA (ALK3), a type I serine/threonine kinase receptor for bone morphogenetic proteins that transduces signals through SMAD1/5/9 to regulate transcriptional programs controlling embryonic patterning, osteogenic and chondrogenic differentiation, and tissue homeostasis. Upon ligand-dependent complex formation with type II BMP receptors, BMPR-IA drives canonical BMP/TGF-β pathway signaling as well as context-dependent cross-talk with MAPK cascades that influence proliferation, apoptosis, and lineage commitment. In mice, altered Bmpr1a activity disrupts developmental morphogenesis and skeletal remodeling and is used to model pathway dysfunction relevant to congenital malformations, fibrosis-associated remodeling, and bone biology. These features make BMPR-IA a central node for dissecting BMP-dependent cell fate decisions in development and disease-relevant cellular phenotypes.
BMPR-IA Double Nickase Plasmid (m) consists of a matched pair of plasmids engineered for high-specificity editing of the Bmpr1a locus in mouse cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within Bmpr1a. 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 Bmpr1a 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 Bmpr1a-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.