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.
AHRR Double Nickase Plasmid (h): sc-412812-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- AHRR 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
- AHRR Double Nickase Plasmid (h) and AHRR Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting AHRR. One or both designs may be available
- Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: AHRR Antibody (5G11): sc-293297
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
AHRR Double Nickase Plasmid (h) | sc-412812-NIC | 20 µg | $410.00 | |||
AHRR Double Nickase Plasmid (h2) | sc-412812-NIC-2 | 20 µg | $410.00 |
Human AHRR (aryl-hydrocarbon receptor repressor) encodes a ligand-inducible transcriptional regulator that attenuates AHR signaling via feedback inhibition, shaping xenobiotic metabolism and cellular stress responses. By competing for ARNT and recruiting corepressor complexes, AHRR modulates transcriptional programs linked to CYP1 family induction, oxidative stress, and inflammatory gene expression. AHRR activity intersects with pathways governing epithelial differentiation, immune modulation, and environmental response, making it relevant for studying how exposure-responsive transcriptional networks contribute to disease-associated phenotypes. Altered AHRR regulation and methylation status have been associated with exposure-related transcriptional signatures and has been investigated in contexts including cancer biology, pulmonary disease mechanisms, and immune dysregulation.
AHRR Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the AHRR locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within AHRR. 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 AHRR 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 AHRR-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.