DABP Double Nickase Plasmid (h): sc-405222-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- DABP 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
- DABP Double Nickase Plasmid (h) and DABP Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting DBP. One or both designs may be available
- Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: DABP Antibody (H-6): sc-390146
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
DABP Double Nickase Plasmid (h) | sc-405222-NIC | 20 µg | $410.00 | |||
DABP Double Nickase Plasmid (h2) | sc-405222-NIC-2 | 20 µg | $410.00 |
DBP encodes the D-site of albumin promoter binding protein (DABP), a PAR bZIP transcription factor that binds D-box elements to coordinate circadian transcriptional programs. In human cells, DABP participates in clock-controlled regulation of metabolic and detoxification gene networks and interfaces with transcriptional oscillators through interactions with core circadian regulators. DBP-dependent rhythms influence hepatic gene expression, hormone signaling, and xenobiotic metabolism, linking this factor to systemic homeostasis. Altered DBP expression or circadian misalignment has been associated with dysregulated metabolic pathways and inflammatory states, supporting its use as a molecular entry point for studying clock-related phenotypes in disease-relevant models.
DABP Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the DBP locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within DBP. 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 DBP 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 DBP-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.