M-Ras Double Nickase Plasmid (h): sc-405471-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- M-Ras 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
- M-Ras Double Nickase Plasmid (h) and M-Ras Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting MRAS. One or both designs may be available
- Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: M-Ras Antibody (C-8): sc-518225
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
M-Ras Double Nickase Plasmid (h) | sc-405471-NIC | 20 µg | $410.00 | |||
M-Ras Double Nickase Plasmid (h2) | sc-405471-NIC-2 | 20 µg | $410.00 |
MRAS encodes M-Ras, a small GTPase of the RAS superfamily that functions as a molecular switch linking extracellular cues to intracellular signaling. In its GTP-bound state, M-Ras engages effectors that intersect with MAPK/ERK and PI3K-related pathways, influencing cell proliferation, differentiation, adhesion, and cytoskeletal organization. MRAS activity integrates receptor-driven signaling and contributes to context-dependent regulation of developmental and immune-associated processes. Dysregulation of RAS-family signaling is broadly relevant to oncogenic and neurodevelopmental mechanisms, making MRAS a useful node for pathway dissection in human cell models.
M-Ras Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the MRAS locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within MRAS. 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 MRAS 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 MRAS-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.