GRAMD1A Double Nickase Plasmid (h): sc-408934-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- GRAMD1A 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
- GRAMD1A Double Nickase Plasmid (h) and GRAMD1A Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting GRAMD1A. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
GRAMD1A Double Nickase Plasmid (h) | sc-408934-NIC | 20 µg | $410.00 | |||
GRAMD1A Double Nickase Plasmid (h2) | sc-408934-NIC-2 | 20 µg | $410.00 |
GRAMD1A encodes a GRAM domain–containing lipid transfer protein localized at endoplasmic reticulum–plasma membrane contact sites, where it contributes to nonvesicular cholesterol transport and membrane lipid homeostasis. By sensing accessible cholesterol and coordinating sterol movement, GRAMD1A supports membrane composition, signaling competence, and organelle communication, linking lipid availability to cellular stress responses. These processes intersect with pathways controlling membrane trafficking, metabolic adaptation, and cholesterol-dependent signaling microdomains. Dysregulation of cholesterol handling and contact-site biology is frequently associated with cardiometabolic traits and tumor cell membrane remodeling, making GRAMD1A a useful node for mechanistic studies of lipid-driven phenotypes.
GRAMD1A Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the GRAMD1A locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within GRAMD1A. 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 GRAMD1A 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 GRAMD1A-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.