RAET1G Double Nickase Plasmid (h): sc-410520-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- RAET1G 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
- RAET1G Double Nickase Plasmid (h) and RAET1G Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting RAET1G. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
RAET1G Double Nickase Plasmid (h) | sc-410520-NIC | 20 µg | $410.00 | |||
RAET1G Double Nickase Plasmid (h2) | sc-410520-NIC-2 | 20 µg | $410.00 |
RAET1G encodes a cell-surface NKG2D ligand in the RAET1/ULBP family that is induced by cellular stress and engages NKG2D on NK cells and subsets of T cells to promote immune recognition. Its expression links DNA damage responses, inflammatory signaling, and membrane trafficking processes to the activation threshold of cytotoxic lymphocytes. Dysregulated RAET1G has been associated with altered immune surveillance in cancer and with inflammatory microenvironments where stress-ligand induction can modulate tissue immunity. As a result, RAET1G is widely studied in pathways controlling stress-induced immunogenicity, tumor–immune interactions, and regulation of innate-like lymphocyte responses.
RAET1G Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the RAET1G locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within RAET1G. 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 RAET1G 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 RAET1G-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.