
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
Inhibin β-B Double Nickase Plasmid (h) | sc-402060-NIC | 20 µg | $410.00 | |||
Inhibin β-B Double Nickase Plasmid (h2) | sc-402060-NIC-2 | 20 µg | $410.00 |
INHBB encodes the inhibin beta B subunit, which homodimerizes to form activin B or heterodimerizes with other TGF-β superfamily subunits to modulate signaling through SMAD2/3-dependent transcriptional programs. Activin/inhibin balance influences endocrine feedback, reproductive tissue function, and broader control of cell proliferation, differentiation, inflammation, and extracellular matrix remodeling. INHBB-driven activin signaling intersects with pathways governing gonadal development and pituitary regulation, and altered expression has been linked in the literature to dysregulated growth control and tissue remodeling in contexts including reproductive disorders and cancer-related phenotypes. These properties make INHBB a useful target for mechanistic studies of TGF-β family signaling dynamics and context-specific transcriptional responses.
Inhibin β-B Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the INHBB locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within INHBB. 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 INHBB 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 INHBB-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.