SMG8 Double Nickase Plasmid (h): sc-408902-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- SMG8 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
- SMG8 Double Nickase Plasmid (h) and SMG8 Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting SMG8. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
SMG8 Double Nickase Plasmid (h) | sc-408902-NIC | 20 µg | $410.00 | |||
SMG8 Double Nickase Plasmid (h2) | sc-408902-NIC-2 | 20 µg | $410.00 |
SMG8 encodes a core regulatory subunit of the SMG1 kinase complex (SMG1–SMG8–SMG9) that controls phosphorylation of UPF1 and progression of nonsense-mediated mRNA decay (NMD). By modulating NMD efficiency and coupling to translation termination surveillance, SMG8 helps maintain transcriptome quality and influences RNA homeostasis, stress responses, and proteostasis. Perturbation of NMD regulators, including SMG8-associated complex components, can alter the stability of aberrant or regulatory mRNAs, with downstream effects on pathways governing cell growth and differentiation. As a result, SMG8 is frequently studied in the context of gene expression control, RNA decay pathway rewiring, and disease-relevant transcriptome dysregulation.
SMG8 Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the SMG8 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within SMG8. 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 SMG8 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 SMG8-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.