RARα/Retinoic Acid Receptor α Double Nickase Plasmid (h): sc-400529-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- RARα/Retinoic Acid Receptor α 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
- RARα/Retinoic Acid Receptor α Double Nickase Plasmid (h) and RARα/Retinoic Acid Receptor α Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting RARA. One or both designs may be available
- Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: RARα/Retinoic Acid Receptor α Antibody (C-1): sc-515796
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
RARα/Retinoic Acid Receptor α Double Nickase Plasmid (h) | sc-400529-NIC | 20 µg | $410.00 | |||
RARα/Retinoic Acid Receptor α Double Nickase Plasmid (h2) | sc-400529-NIC-2 | 20 µg | $410.00 |
RARA encodes RARα, a ligand-activated nuclear receptor that heterodimerizes with RXR to bind retinoic acid response elements and regulate transcriptional programs controlling cell fate decisions. Through retinoid signaling, RARα coordinates processes including embryonic development, epithelial differentiation, cell-cycle control, and chromatin remodeling in a context-dependent manner. RARα activity is shaped by ligand availability and coregulator exchange, linking it to pathways governing transcriptional repression/activation and lineage commitment. Dysregulation of RARA-dependent transcription and receptor signaling has been associated with altered differentiation states and oncogenic transcriptional programs in hematopoietic and solid-tissue settings, supporting its relevance in disease mechanism studies.
RARα/Retinoic Acid Receptor α Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the RARA locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within RARA. 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 RARA 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 RARA-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.