ERAB Double Nickase Plasmid (h): sc-405211-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- ERAB 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
- ERAB Double Nickase Plasmid (h) and ERAB Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting HSD17B10. One or both designs may be available
- Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: ERAB Antibody (E-10): sc-393693
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
ERAB Double Nickase Plasmid (h) | sc-405211-NIC | 20 µg | $410.00 | |||
ERAB Double Nickase Plasmid (h2) | sc-405211-NIC-2 | 20 µg | $410.00 |
HSD17B10 encodes ERAB, a multifunctional mitochondrial enzyme also known as 17β-hydroxysteroid dehydrogenase type 10 that participates in short-chain fatty acid and amino acid catabolism. ERAB is a component of the mitochondrial RNase P complex, supporting tRNA processing and broader mitochondrial gene expression and oxidative phosphorylation. Through its roles in mitochondrial metabolism and proteostasis, ERAB influences redox balance and cellular energy homeostasis in metabolically active tissues. Altered HSD17B10/ERAB function has been associated with mitochondrial dysfunction and neurodegeneration-relevant phenotypes, making it useful for studying mechanisms that couple mitochondrial metabolism to cellular stress responses.
ERAB Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the HSD17B10 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within HSD17B10. 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 HSD17B10 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 HSD17B10-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.