RIP Double Nickase Plasmid (h): sc-400377-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- RIP 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
- RIP Double Nickase Plasmid (h) and RIP Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting RIPK1. One or both designs may be available
- Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: RIP Antibody (C-12): sc-133102
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
RIP Double Nickase Plasmid (h) | sc-400377-NIC | 20 µg | $410.00 | |||
RIP Double Nickase Plasmid (h2) | sc-400377-NIC-2 | 20 µg | $410.00 |
Human RIPK1 (RIP) is a serine/threonine kinase that integrates signals from TNF receptor and pattern-recognition pathways to coordinate inflammatory signaling and programmed cell death decisions. Through assembly of receptor-associated complexes, RIPK1 regulates NF-κB and MAPK activation as well as apoptosis and necroptosis via crosstalk with FADD–caspase-8 and RIPK3–MLKL signaling. Its kinase-dependent and scaffold functions shape cytokine production, innate immune responses, and cellular stress adaptation. Dysregulated RIPK1 activity has been implicated in inflammatory and neurodegenerative disease mechanisms and in tumor microenvironment biology, making it a frequent target for mechanistic studies of cell fate control.
RIP Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the RIPK1 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within RIPK1. 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 RIPK1 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 RIPK1-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.