FAM103A1 Double Nickase Plasmid (h): sc-418204-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- FAM103A1 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
- FAM103A1 Double Nickase Plasmid (h) and FAM103A1 Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting FAM103A1. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
FAM103A1 Double Nickase Plasmid (h) | sc-418204-NIC | 20 µg | $410.00 | |||
FAM103A1 Double Nickase Plasmid (h2) | sc-418204-NIC-2 | 20 µg | $410.00 |
FAM103A1 (family with sequence similarity 103 member A1) encodes a poorly characterized human protein with limited functional annotation, making it of interest for systematic gene-function discovery. Available evidence suggests a role in basic cellular homeostasis, potentially influencing processes such as RNA/protein handling or cell-cycle–linked regulation through currently unresolved interaction networks. Because genes of unknown function can contribute to context-dependent phenotypes, FAM103A1 is frequently evaluated in genome-scale perturbation datasets for effects on proliferation, stress responses, and lineage-specific dependencies. Defining FAM103A1 activity can help clarify pathways that become dysregulated in disease-relevant cellular states without implying clinical utility.
FAM103A1 Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the FAM103A1 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within FAM103A1. 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 FAM103A1 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 FAM103A1-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.