RASA4B Double Nickase Plasmid (h): sc-418861-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- RASA4B 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
- RASA4B Double Nickase Plasmid (h) and RASA4B Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting RASA4B. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
RASA4B Double Nickase Plasmid (h) | sc-418861-NIC | 20 µg | $410.00 | |||
RASA4B Double Nickase Plasmid (h2) | sc-418861-NIC-2 | 20 µg | $410.00 |
RASA4B encodes a Ras GTPase-activating protein that promotes conversion of active Ras-GTP to inactive Ras-GDP, acting as a negative regulator of Ras-dependent signaling. By attenuating upstream inputs into MAPK/ERK and PI3K-AKT cascades, RASA4B helps shape cellular programs that govern proliferation, differentiation, and stress-responsive signaling dynamics. Dysregulated Ras pathway control is broadly implicated in oncogenic transformation and altered immune and inflammatory signaling, making RASA4B a useful node for interrogating pathway tuning in disease-relevant models. Mapping RASA4B function can clarify how Ras signal amplitude and duration influence transcriptional outputs and cell-state transitions.
RASA4B Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the RASA4B locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within RASA4B. 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 RASA4B 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 RASA4B-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.