FSHR Double Nickase Plasmid (h): sc-400899-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- FSHR 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
- FSHR Double Nickase Plasmid (h) and FSHR Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting FSHR. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
FSHR Double Nickase Plasmid (h) | sc-400899-NIC | 20 µg | $410.00 | |||
FSHR Double Nickase Plasmid (h2) | sc-400899-NIC-2 | 20 µg | $410.00 |
Follicle stimulating hormone receptor (FSHR) is a G protein–coupled receptor predominantly expressed in gonadal somatic cells, where binding of follicle-stimulating hormone activates Gαs/adenylyl cyclase signaling to elevate cAMP and engage PKA-dependent transcriptional programs. Downstream effects include modulation of steroidogenesis, cell proliferation, differentiation, and survival through coordinated signaling with MAPK/ERK and PI3K/AKT pathways. In human biology, FSHR function is central to regulation of folliculogenesis and spermatogenesis, linking receptor activity to reproductive endocrinology and hormone-responsive cellular states. Altered FSHR expression or signaling has been studied in the context of infertility phenotypes, ovarian dysfunction, and endocrine pathway dysregulation relevant to reproductive system research.
FSHR Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the FSHR locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within FSHR. 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 FSHR 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 FSHR-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.