ACTR-IB Double Nickase Plasmid (h): sc-401943-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- ACTR-IB 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
- ACTR-IB Double Nickase Plasmid (h) and ACTR-IB Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting ACVR1B. One or both designs may be available
- Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: ACTR-IB Antibody (ALEX66): sc-73677
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
ACTR-IB Double Nickase Plasmid (h) | sc-401943-NIC | 20 µg | $410.00 | |||
ACTR-IB Double Nickase Plasmid (h2) | sc-401943-NIC-2 | 20 µg | $410.00 |
ACVR1B encodes activin receptor type-1B (ACTR-IB/ALK4), a serine/threonine kinase receptor in the TGF-β superfamily that transduces activin and related ligands to regulate cell fate decisions. Upon ligand binding, ACTR-IB forms receptor complexes that phosphorylate SMAD2/3, driving transcriptional programs controlling proliferation, differentiation, and apoptosis, with crosstalk to MAPK and PI3K signaling. This pathway is central to developmental patterning, tissue homeostasis, and immune and endocrine regulation, and dysregulation of activin/TGF-β signaling has been implicated in fibrosis, tumor biology, and reproductive and metabolic disorders.
ACTR-IB Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the ACVR1B locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within ACVR1B. 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 ACVR1B 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 ACVR1B-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.