Not CRISPR data: the image illustrates antibody quality for visualizing CRISPR experiment results.
Not CRISPR data: the image illustrates antibody quality for visualizing CRISPR experiment results.
CPTI-M Double Nickase Plasmid (h): sc-401456-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- CPTI-M 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
- CPTI-M Double Nickase Plasmid (h) and CPTI-M Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting CPT1B. One or both designs may be available
- Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: CPTI-M Antibody (D-8): sc-515709
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
CPTI-M Double Nickase Plasmid (h) | sc-401456-NIC | 20 µg | $410.00 | |||
CPTI-M Double Nickase Plasmid (h2) | sc-401456-NIC-2 | 20 µg | $410.00 |
CPT1B encodes carnitine palmitoyltransferase 1B (CPTI-M), the muscle-associated outer mitochondrial membrane enzyme that catalyzes the rate-limiting formation of long-chain acylcarnitines for import into mitochondria and subsequent β-oxidation. By controlling fatty acid entry into the mitochondrial matrix, CPTI-M helps regulate lipid catabolism, energy homeostasis, and substrate switching between fatty acids and glucose, integrating with AMPK signaling, PPAR-driven metabolic transcription programs, and malonyl-CoA–mediated control of fatty acid flux. Altered CPT1B activity or expression has been linked to dysregulated fatty acid oxidation, lipotoxic stress, and metabolic remodeling that is relevant to cardiometabolic phenotypes and muscle energetics. In research settings, CPT1B is commonly examined in the context of mitochondrial function, acylcarnitine profiling, oxidative capacity, and metabolic adaptation to nutrient availability.
CPTI-M Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the CPT1B locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within CPT1B. 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 CPT1B 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 CPT1B-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.