AIM1 Double Nickase Plasmid (h): sc-410680-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- AIM1 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
- AIM1 Double Nickase Plasmid (h) and AIM1 Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting AIM1. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
AIM1 Double Nickase Plasmid (h) | sc-410680-NIC | 20 µg | $410.00 | |||
AIM1 Double Nickase Plasmid (h2) | sc-410680-NIC-2 | 20 µg | $410.00 |
AIM1 (absent in melanoma 1) encodes a non-lens βγ-crystallin–like protein implicated in cytoskeletal organization and cellular differentiation. In epithelial contexts, AIM1 has been linked to actin-associated structures and maintenance of cell morphology, processes that influence adhesion and motility programs. Altered AIM1 expression has been reported across multiple tumor types and is frequently studied in relation to transcriptional regulation and epigenetic silencing mechanisms that accompany malignant progression. These features make AIM1 a useful locus for interrogating pathways governing cell structure, lineage state, and context-dependent tumor biology.
AIM1 Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the AIM1 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within AIM1. 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 AIM1 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 AIM1-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.