SMG5 Double Nickase Plasmid (h): sc-406989-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- SMG5 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
- SMG5 Double Nickase Plasmid (h) and SMG5 Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting SMG5. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
SMG5 Double Nickase Plasmid (h) | sc-406989-NIC | 20 µg | $410.00 | |||
SMG5 Double Nickase Plasmid (h2) | sc-406989-NIC-2 | 20 µg | $410.00 |
SMG5 encodes a conserved core factor of the nonsense-mediated mRNA decay (NMD) pathway that helps eliminate transcripts containing premature termination codons and modulates the stability of select physiological mRNAs. SMG5 associates with phosphorylated UPF1 and cooperates with PP2A-containing complexes to promote UPF1 dephosphorylation, coordinating the transition from surveillance to mRNA decay. Through these activities, SMG5 contributes to translation-dependent RNA quality control, proteostasis, and regulation of gene expression programs during cellular stress responses. Dysregulation of NMD components, including SMG5, has been linked to altered transcriptome homeostasis and phenotypes relevant to neurodevelopmental and cancer biology, making SMG5 a useful node for mechanistic studies of RNA surveillance.
SMG5 Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the SMG5 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within SMG5. 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 SMG5 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 SMG5-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.