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.
V-ATPase B1 Double Nickase Plasmid (h): sc-400926-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- V-ATPase B1 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
- V-ATPase B1 Double Nickase Plasmid (h) and V-ATPase B1 Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting ATP6V1B1. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
V-ATPase B1 Double Nickase Plasmid (h) | sc-400926-NIC | 20 µg | $410.00 | |||
V-ATPase B1 Double Nickase Plasmid (h2) | sc-400926-NIC-2 | 20 µg | $410.00 |
ATP6V1B1 encodes the B1 subunit of the V1 domain of vacuolar H+-ATPase (V-ATPase), a multi-subunit proton pump that drives ATP-dependent acidification of intracellular compartments and specialized plasma membrane domains. V-ATPase activity supports vesicular trafficking, receptor recycling, lysosomal degradation, endosome maturation, and pH-dependent protein processing, linking ATP6V1B1 to organelle homeostasis and epithelial transport physiology. In human kidney and inner ear epithelia, B1-containing V-ATPase complexes contribute to transepithelial proton secretion and pH regulation, integrating with pathways that control electrolyte balance and acid–base homeostasis. Dysregulation or genetic disruption of ATP6V1B1 is associated with disorders of renal tubular function and hearing, making it a relevant target for mechanistic studies of proton transport and epithelial physiology.
V-ATPase B1 Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the ATP6V1B1 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within ATP6V1B1. 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 ATP6V1B1 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 ATP6V1B1-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.