FAM98A Double Nickase Plasmid (h): sc-411841-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- FAM98A 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
- FAM98A Double Nickase Plasmid (h) and FAM98A Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting FAM98A. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
FAM98A Double Nickase Plasmid (h) | sc-411841-NIC | 20 µg | $410.00 | |||
FAM98A Double Nickase Plasmid (h2) | sc-411841-NIC-2 | 20 µg | $410.00 |
FAM98A encodes a conserved, RNA-binding protein implicated in ribonucleoprotein complex biology and the coordination of RNA processing with protein homeostasis. It has been linked to the regulation of translation and intracellular trafficking of RNA–protein assemblies, and is frequently studied in the context of cellular stress responses and growth control. Altered FAM98A expression has been reported across multiple disease-associated transcriptomic datasets, supporting investigation of its contribution to dysregulated proliferation and proteostasis in human cells. Functional interrogation of FAM98A is therefore relevant to pathways governing RNA metabolism, cell cycle progression, and adaptive stress signaling.
FAM98A Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the FAM98A locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within FAM98A. 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 FAM98A 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 FAM98A-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.