TNF-R1 Double Nickase Plasmid (m2): sc-423442-NIC-2
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- TNF-R1 Double Nickase Plasmid (m2) 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
- TNF-R1 Double Nickase Plasmid (m2) and TNF-R1 Double Nickase Plasmid (m22) encode distinct paired gRNA designs targeting Tnfrsf1a. One or both designs may be available
- Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: TNF-R1 Antibody (H-5): sc-8436
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
TNF-R1 Double Nickase Plasmid (m2) | sc-423442-NIC-2 | 20 µg | $410.00 |
Mouse Tnfrsf1a encodes tumor necrosis factor receptor 1 (TNF‑R1), a ubiquitously expressed TNF receptor that binds TNF and initiates signal transduction controlling inflammation, cell survival, and programmed cell death. Upon ligand engagement, TNF‑R1 assembles membrane and cytosolic signaling complexes that regulate NF‑κB and MAPK activation as well as caspase-dependent apoptosis and RIPK-mediated necroptosis, linking innate immune cues to transcriptional and death pathways. Dysregulation of TNF‑R1 signaling is implicated in inflammatory and autoimmune pathophysiology, neuroinflammatory processes, and tissue injury responses, making Tnfrsf1a a key node for studying cytokine-driven homeostasis. Gene editing of Tnfrsf1a in mouse models supports mechanistic interrogation of TNF signaling networks, receptor domain function, and cell-type–specific contributions to immune-mediated disease phenotypes.
TNF-R1 Double Nickase Plasmid (m2) consists of a matched pair of plasmids engineered for high-specificity editing of the Tnfrsf1a locus in mouse cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within Tnfrsf1a. 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 Tnfrsf1a 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 Tnfrsf1a-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.