
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
CPTII CRISPR Activation Plasmid (h) | sc-403401-ACT | 20 µg | $397.00 |
Human CPT2 encodes carnitine palmitoyltransferase II (CPTII), a mitochondrial inner membrane enzyme that catalyzes the reconversion of long-chain acylcarnitines to acyl-CoA, enabling entry into the β-oxidation spiral. This step is essential for mitochondrial fatty acid oxidation and energy homeostasis in high-demand tissues, linking CPTII activity to ketogenesis, ATP production, and metabolic stress responses. Altered CPT2 function disrupts long-chain fatty acid utilization and is associated with inborn errors of metabolism characterized by impaired fatty acid oxidation, particularly under fasting, illness, or increased energy demand. CPT2 is therefore widely studied in pathways governing mitochondrial metabolism, lipid handling, and cellular bioenergetics.
CPTII CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous CPT2 expression without altering the underlying DNA sequence.
CPTII CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the CPT2 locus in human cell lines. The system is built around a catalytically inactive Cas9 (dCas9) carrying two inactivating mutations (D10A and N863A) that eliminate nuclease activity while preserving DNA binding. This dCas9 is fused to VP64, a potent transcriptional activator, and is co-expressed with a blasticidin resistance gene for selection. The second plasmid encodes the MS2-p65-HSF1 fusion protein, a secondary activator complex that works in concert with dCas9-VP64, alongside a hygromycin resistance gene. The third plasmid encodes a target-specific 20 nt sgRNA fused to two MS2 RNA aptamers that recruit the MS2-p65-HSF1 complex to the activation site, accompanied by a puromycin resistance gene. The three plasmids are delivered at a 1:1:1 mass ratio for balanced expression of all system components.
Once assembled at the target locus, the SAM complex binds within approximately 200 bp upstream of the CPT2 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous CPTII expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native CPT2 locus and enabling the study of CPTII-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of CPTII pathway restoration in tumor cells with silenced or reduced CPT2 expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.