Ah Receptor Double Nickase Plasmid (h): sc-400297-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- Ah Receptor 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
- Ah Receptor Double Nickase Plasmid (h) and Ah Receptor Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting AHR. One or both designs may be available
- Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: Ah Receptor Antibody (A-3): sc-133088
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
Ah Receptor Double Nickase Plasmid (h) | sc-400297-NIC | 20 µg | $410.00 | |||
Ah Receptor Double Nickase Plasmid (h2) | sc-400297-NIC-2 | 20 µg | $410.00 |
Human AHR encodes the aryl hydrocarbon receptor (Ah Receptor), a ligand-activated transcription factor that senses xenobiotics and endogenous metabolites to regulate gene expression programs controlling detoxification, barrier function, and immune modulation. Upon ligand binding, AHR translocates to the nucleus, heterodimerizes with ARNT, and binds xenobiotic response elements to induce targets such as CYP1A1 and CYP1B1, intersecting with oxidative stress responses and inflammatory signaling. AHR activity integrates with pathways including NF-κB, WNT/β-catenin, and TGF-β, influencing cell cycle control, differentiation, and tissue homeostasis. Dysregulated AHR signaling has been implicated in context-dependent tumor biology, chronic inflammatory states, and altered responses to environmental exposures, supporting its utility as a mechanistic node in toxicology and immunology research.
Ah Receptor Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the AHR locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within AHR. 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 AHR 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 AHR-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.