SPRED2 Double Nickase Plasmid (m): sc-431133-NIC
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- SPRED2 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
- SPRED2 Double Nickase Plasmid (m) and SPRED2 Double Nickase Plasmid (m2) encode distinct paired gRNA designs targeting Spred2. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
SPRED2 Double Nickase Plasmid (m) | sc-431133-NIC | 20 µg | $410.00 | |||
SPRED2 Double Nickase Plasmid (m2) | sc-431133-NIC-2 | 20 µg | $410.00 |
Spred2 encodes SPRED2, a Sprouty-related adaptor protein that negatively regulates receptor tyrosine kinase signaling by restraining the RAS–RAF–MEK–ERK/MAPK cascade. By recruiting neurofibromin (NF1) to activated RAS and modulating growth factor–driven phosphorylation programs, SPRED2 influences cell proliferation, differentiation, and migration in multiple mouse tissues. Dysregulated SPRED2 activity has been linked to aberrant MAPK signaling states relevant to inflammatory phenotypes and oncogenic signaling contexts, making it a useful node for studying pathway feedback and signal amplitude control. In mouse models, Spred2 perturbation is commonly applied to dissect ERK-dependent transcriptional responses and cross-talk with cytokine and immune signaling networks.
SPRED2 Double Nickase Plasmid (m) consists of a matched pair of plasmids engineered for high-specificity editing of the Spred2 locus in mouse cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within Spred2. 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 Spred2 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 Spred2-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.