HMGCR Double Nickase Plasmid (h): sc-400560-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- HMGCR 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
- HMGCR Double Nickase Plasmid (h) and HMGCR Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting HMGCR. One or both designs may be available
- Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: HMGCR Antibody (C-1): sc-271595
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
HMGCR Double Nickase Plasmid (h) | sc-400560-NIC | 20 µg | $410.00 | |||
HMGCR Double Nickase Plasmid (h2) | sc-400560-NIC-2 | 20 µg | $410.00 |
HMGCR encodes 3-hydroxy-3-methylglutaryl-CoA reductase, the rate-limiting enzyme of the mevalonate pathway that converts HMG-CoA to mevalonate and governs de novo cholesterol biosynthesis. By controlling flux through sterol and isoprenoid production, HMGCR influences membrane biogenesis, protein prenylation, and signaling outputs linked to cell growth and metabolic adaptation. HMGCR activity is tightly regulated by SREBP-dependent transcription, sterol-sensing feedback, and ER-associated degradation, integrating lipid availability with cellular homeostasis. Dysregulation of mevalonate pathway enzymes, including HMGCR, is frequently examined in studies of hypercholesterolemia, atherosclerosis risk mechanisms, and metabolic rewiring in cancer and inflammatory states.
HMGCR Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the HMGCR locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within HMGCR. 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 HMGCR 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 HMGCR-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.