RASAL3 Double Nickase Plasmid (h): sc-404999-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- RASAL3 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
- RASAL3 Double Nickase Plasmid (h) and RASAL3 Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting RASAL3. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
RASAL3 Double Nickase Plasmid (h) | sc-404999-NIC | 20 µg | $410.00 | |||
RASAL3 Double Nickase Plasmid (h2) | sc-404999-NIC-2 | 20 µg | $410.00 |
RASAL3 encodes a Ras GTPase-activating protein that attenuates Ras signaling by accelerating GTP hydrolysis on Ras-family small GTPases, thereby constraining downstream MAPK/ERK and PI3K–AKT pathway output. In immune-lineage cells, RASAL3 is implicated in calibrating antigen receptor–proximal signaling, influencing activation thresholds, proliferation, and differentiation programs. By shaping Ras-dependent transcriptional and metabolic responses, RASAL3 can affect cellular stress responses and survival decisions. Dysregulated Ras pathway control is broadly relevant to immune dysfunction and oncogenic signaling contexts, making RASAL3 a useful node for mechanistic studies of signal transduction.
RASAL3 Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the RASAL3 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within RASAL3. 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 RASAL3 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 RASAL3-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.