LONRF2 Double Nickase Plasmid (h): sc-414877-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- LONRF2 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
- LONRF2 Double Nickase Plasmid (h) and LONRF2 Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting LONRF2. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
LONRF2 Double Nickase Plasmid (h) | sc-414877-NIC | 20 µg | $410.00 |
LONRF2 encodes a Lon peptidase N‑terminal domain and RING finger protein that is predicted to act as an E3 ubiquitin ligase, linking substrate recognition to ubiquitin-dependent protein turnover. Through its RING-type domain, LONRF2 is positioned to influence proteostasis pathways that regulate protein stability, quality control, and stress-adaptive signaling in human cells. Modulation of ubiquitination networks can affect cell-cycle progression, neuronal and immune signaling, and responses to proteotoxic stress, making LONRF2 a useful target for mechanistic studies of pathway regulation. Altered ubiquitin-mediated regulation is broadly implicated in human disease biology, supporting research into how LONRF2 impacts cellular phenotypes relevant to complex disorders.
LONRF2 Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the LONRF2 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within LONRF2. 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 LONRF2 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 LONRF2-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.