FAM73B Double Nickase Plasmid (h): sc-413719-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- FAM73B 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
- FAM73B Double Nickase Plasmid (h) and FAM73B Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting MIGA2. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
FAM73B Double Nickase Plasmid (h) | sc-413719-NIC | 20 µg | $410.00 |
MIGA2 (FAM73B) encodes a mitochondrial outer membrane protein that contributes to mitochondrial morphology by promoting organelle fusion and maintaining network integrity. Through its role in mitochondrial dynamics, FAM73B influences energy metabolism, reactive oxygen species homeostasis, and crosstalk between mitochondria and the endoplasmic reticulum that can affect cellular stress responses. Perturbation of mitochondrial fusion–fission balance is implicated in metabolic dysregulation and broader processes such as apoptosis and innate immune signaling. Altered FAM73B activity has been studied in the context of mitochondrial dysfunction-associated phenotypes relevant to cancer cell metabolism and neurobiology.
FAM73B Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the MIGA2 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within MIGA2. 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 MIGA2 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 MIGA2-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.