17β-HSD3 Double Nickase Plasmid (h): sc-403863-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- 17β-HSD3 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
- 17β-HSD3 Double Nickase Plasmid (h) and 17β-HSD3 Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting HSD17B3. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
17β-HSD3 Double Nickase Plasmid (h) | sc-403863-NIC | 20 µg | $410.00 | |||
17β-HSD3 Double Nickase Plasmid (h2) | sc-403863-NIC-2 | 20 µg | $410.00 |
HSD17B3 encodes human 17β-HSD3, a microsomal oxidoreductase that catalyzes the NADPH-dependent conversion of androstenedione to testosterone, a key step in androgen biosynthesis. This enzyme functions within steroid hormone metabolic networks that shape androgen receptor signaling and downstream transcriptional programs affecting sexual development and reproductive physiology. HSD17B3 activity contributes to tissue-specific androgen availability through intracrine steroid metabolism and intersects with broader pathways governing steroidogenic flux and redox balance. Altered HSD17B3 function or expression is studied in the context of disorders of sex development and androgen-dependent endocrine phenotypes, as well as mechanisms of steroid metabolism in gonadal and peripheral tissues.
17β-HSD3 Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the HSD17B3 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within HSD17B3. 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 HSD17B3 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 HSD17B3-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.