CSH1 Double Nickase Plasmid (h): sc-401213-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- CSH1 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
- CSH1 Double Nickase Plasmid (h) and CSH1 Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting CSH1. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
CSH1 Double Nickase Plasmid (h) | sc-401213-NIC | 20 µg | $410.00 | |||
CSH1 Double Nickase Plasmid (h2) | sc-401213-NIC-2 | 20 µg | $410.00 |
CSH1 encodes chorionic somatomammotropin hormone 1 (placental lactogen), a secreted peptide hormone produced predominantly by syncytiotrophoblasts in the human placenta. CSH1 contributes to maternal–fetal metabolic adaptation by modulating insulin sensitivity, lipid mobilization, and nutrient partitioning during pregnancy through signaling pathways related to prolactin and growth hormone receptor family activity. Its expression is tightly linked to trophoblast differentiation, placental endocrine function, and regulation of fetal growth trajectories. Dysregulated CSH1 expression has been associated with placental insufficiency phenotypes and pregnancy-related disorders, including altered fetal growth and metabolic complications, making it relevant for studies of placental development and endocrine signaling.
CSH1 Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the CSH1 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within CSH1. 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 CSH1 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 CSH1-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.