Not CRISPR data: the image illustrates antibody quality for visualizing CRISPR experiment results.
Not CRISPR data: the image illustrates antibody quality for visualizing CRISPR experiment results.
ACTR-IIB Double Nickase Plasmid (m): sc-418977-NIC
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- ACTR-IIB 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
- ACTR-IIB Double Nickase Plasmid (m) and ACTR-IIB Double Nickase Plasmid (m2) encode distinct paired gRNA designs targeting Acvr2b. One or both designs may be available
- Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: ACTR-IIB Antibody (G-7): sc-376593
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
ACTR-IIB Double Nickase Plasmid (m) | sc-418977-NIC | 20 µg | $410.00 | |||
ACTR-IIB Double Nickase Plasmid (m2) | sc-418977-NIC-2 | 20 µg | $410.00 |
Acvr2b encodes activin receptor type IIB (ACTR-IIB), a transmembrane serine/threonine kinase that binds TGF-β superfamily ligands such as myostatin (GDF8), activins, and related growth factors. Upon ligand engagement, ACTR-IIB forms signaling complexes with type I receptors to activate SMAD2/3-dependent transcriptional programs that regulate skeletal muscle mass, adipose biology, fibrosis, and cellular differentiation. In mouse systems, Acvr2b signaling is widely used to study tissue growth control and remodeling across muscle and metabolic pathways, as well as context-dependent inflammatory and extracellular matrix responses. Dysregulated ACTR-IIB pathway activity has been associated with muscle wasting phenotypes and altered energy homeostasis, making it a relevant node for mechanistic studies in neuromuscular and metabolic disease models.
ACTR-IIB Double Nickase Plasmid (m) consists of a matched pair of plasmids engineered for high-specificity editing of the Acvr2b locus in mouse cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within Acvr2b. 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 Acvr2b 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 Acvr2b-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.