ELOVL6 CRISPR Activation Plasmid (h): sc-413125-ACT

ELOVL6 (elongation of very long chain fatty acids protein 6) is a microsomal fatty acid elongase that catalyzes the extension of saturated and monounsaturated C12–C16 fatty acids to longer-chain species such as stearate (C18:0) within the endoplasmic reticulum. By shaping the cellular pool of long-chain acyl-CoAs, ELOVL6 influences de novo lipogenesis, membrane lipid composition, and downstream glycerolipid and sphingolipid biosynthesis. ELOVL6 activity intersects with metabolic signaling networks including SREBP1-driven transcriptional programs and lipid-mediated stress responses that modulate insulin sensitivity and inflammation. Altered ELOVL6 expression has been associated with dysregulated lipid homeostasis observed in metabolic disease phenotypes, including hepatic steatosis, obesity-related insulin resistance, and cardiometabolic risk states.

ELOVL6 CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous ELOVL6 expression without altering the underlying DNA sequence.

ELOVL6 CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the ELOVL6 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 ELOVL6 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous ELOVL6 expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native ELOVL6 locus and enabling the study of ELOVL6-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of ELOVL6 pathway restoration in tumor cells with silenced or reduced ELOVL6 expression.

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