PRMT3 Double Nickase Plasmid (h): sc-406688-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- PRMT3 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
- PRMT3 Double Nickase Plasmid (h) and PRMT3 Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting PRMT3. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
PRMT3 Double Nickase Plasmid (h) | sc-406688-NIC | 20 µg | $410.00 | |||
PRMT3 Double Nickase Plasmid (h2) | sc-406688-NIC-2 | 20 µg | $410.00 |
PRMT3 encodes protein arginine methyltransferase 3, a cytosolic type I PRMT that catalyzes asymmetric dimethylation of arginine residues on protein substrates, shaping protein–protein interactions and post-transcriptional regulation. PRMT3 is implicated in ribosome biogenesis and translational control through methylation of ribosomal and RNA-associated factors, linking it to proteostasis and cellular growth programs. By modulating signaling and RNA metabolism, PRMT3 can influence stress responses and differentiation states in a context-dependent manner. Altered PRMT3 expression or activity has been associated with dysregulated proliferation and metabolic phenotypes reported in multiple disease-relevant models, supporting its study in mechanistic research.
PRMT3 Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the PRMT3 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within PRMT3. 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 PRMT3 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 PRMT3-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.