ACAD-11 CRISPR Activation Plasmid (h): sc-408606-ACT

Human ACAD11 encodes acyl-CoA dehydrogenase family member 11 (ACAD-11), a mitochondrial enzyme implicated in the initiation of fatty acid β-oxidation through FAD-dependent dehydrogenation of specific acyl-CoA substrates. By contributing to mitochondrial lipid catabolism, ACAD-11 influences cellular energy balance, redox homeostasis, and lipid signaling pathways that intersect with PPAR-regulated metabolic programs. Altered ACAD11 expression or activity is therefore relevant to studies of mitochondrial dysfunction, lipid accumulation, and metabolic stress responses. In biomedical research settings, ACAD11 is frequently evaluated in contexts linking fatty acid oxidation capacity with inflammation, neurobiology, and metabolic disease-associated phenotypes.

ACAD-11 CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous ACAD11 expression without altering the underlying DNA sequence.

ACAD-11 CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the ACAD11 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 ACAD11 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous ACAD-11 expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native ACAD11 locus and enabling the study of ACAD-11-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of ACAD-11 pathway restoration in tumor cells with silenced or reduced ACAD11 expression.

For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.