FAM46A Double Nickase Plasmid (h): sc-410014-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- FAM46A 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
- FAM46A Double Nickase Plasmid (h) and FAM46A Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting FAM46A. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
FAM46A Double Nickase Plasmid (h) | sc-410014-NIC | 20 µg | $410.00 | |||
FAM46A Double Nickase Plasmid (h2) | sc-410014-NIC-2 | 20 µg | $410.00 |
FAM46A (family with sequence similarity 46 member A, also known as TENT5A) encodes a non-canonical poly(A) polymerase implicated in cytoplasmic mRNA tailing that influences transcript stability and translational output. The protein is linked to post-transcriptional gene regulation programs that shape cell-state transitions, including differentiation-associated changes in secretory and extracellular matrix gene expression. Perturbation of FAM46A has been associated with dysregulated RNA metabolism and altered proteostasis, and genetic or expression changes have been reported in hematologic disease contexts such as multiple myeloma. As a result, FAM46A is frequently studied for its contribution to RNA processing pathways and their downstream effects on cellular phenotype.
FAM46A Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the FAM46A locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within FAM46A. 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 FAM46A 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 FAM46A-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.