ROGDI Double Nickase Plasmid (m): sc-425785-NIC
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- ROGDI Double Nickase Plasmid (m) 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
- ROGDI Double Nickase Plasmid (m) and ROGDI Double Nickase Plasmid (m2) encode distinct paired gRNA designs targeting Rogdi. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
ROGDI Double Nickase Plasmid (m) | sc-425785-NIC | 20 µg | $410.00 | |||
ROGDI Double Nickase Plasmid (m2) | sc-425785-NIC-2 | 20 µg | $410.00 |
Rogdi encodes ROGDI, a conserved protein implicated in maintaining cellular homeostasis through roles linked to nuclear organization and stress-responsive processes. Although its molecular partners are still being defined, ROGDI has been associated with pathways that influence cell viability and neuronal development, consistent with phenotypes reported for RO GDI-related neurodevelopmental disorders. In mouse systems, perturbation of Rogdi provides a tractable route to examine gene-function relationships in the context of tissue maturation and stress signaling. These studies support mechanistic investigations connecting ROGDI dysfunction to developmental pathology without implying clinical outcomes.
ROGDI Double Nickase Plasmid (m) consists of a matched pair of plasmids engineered for high-specificity editing of the Rogdi locus in mouse cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within Rogdi. 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 Rogdi 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 Rogdi-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.