AID Double Nickase Plasmid (h): sc-401542-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- AID 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
- AID Double Nickase Plasmid (h) and AID Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting AICDA. One or both designs may be available
- Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: AID Antibody (H-3): sc-518170
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
AID Double Nickase Plasmid (h) | sc-401542-NIC | 20 µg | $410.00 | |||
AID Double Nickase Plasmid (h2) | sc-401542-NIC-2 | 20 µg | $410.00 |
AICDA encodes activation-induced cytidine deaminase (AID), a DNA-editing enzyme that deaminates cytosine to uracil in single-stranded DNA during transcription. In activated B cells, AID initiates somatic hypermutation and class switch recombination of immunoglobulin genes by coupling lesion formation to base excision repair and mismatch repair pathways, shaping antibody affinity and isotype. Misregulated AID activity can introduce off-target mutations and chromosomal translocations, linking AICDA dysregulation to genomic instability observed in B cell malignancies and other contexts of aberrant DNA damage signaling. As a result, AICDA is widely studied in adaptive immunity, mutagenesis mechanisms, and DNA repair pathway choice.
AID Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the AICDA locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within AICDA. 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 AICDA 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 AICDA-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.