ELOVL2 CRISPR Activation Plasmid (h): sc-404998-ACT
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- ELOVL2 CRISPR Activation Plasmid (h) is a synergistic activation mediator (SAM) transcription activation system designed to specifically upregulate gene expression
- ELOVL2 CRISPR Activation Plasmid (h) consists of three plasmids at a 1:1:1 mass ratio: a plasmid encoding the deactivated Cas9 (dCas9) nuclease (D10A and N863A) fused to the transactivation domain VP64, and a blasticidin resistance gene; a plasmid encoding the MS2-p65-HSF1 fusion protein, and a hygromycin resistance gene; a plasmid encoding a target-specific 20 nt guide RNA fused to two MS2 RNA aptamers, and a puromycin resistance gene
- The resulting SAM complex binds to a site-specific region approximately 200-250 nt upstream of the transcriptional start site and provides robust recruitment of transcription factors for highly efficient gene activation
- gRNAs encoded by ELOVL2 CRISPR Activation Plasmid (h) and ELOVL2 CRISPR Activation Plasmid (h2) target distinct regulatory regions upstream of the ELOVL2 transcriptional start site. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
ELOVL2 CRISPR Activation Plasmid (h) | sc-404998-ACT | 20 µg | $397.00 |
ELOVL2 encodes an endoplasmic reticulum–localized fatty acid elongase that catalyzes rate-limiting elongation steps in the synthesis of very long-chain polyunsaturated fatty acids, including precursors for docosahexaenoic acid (DHA). By extending C20–C22 substrates to longer-chain products, ELOVL2 influences membrane lipid composition, lipid mediator availability, and cellular bioenergetics through interconnected fatty acid metabolism and phospholipid remodeling pathways. Altered ELOVL2 expression or activity has been associated with changes in retinal and neural lipid homeostasis, inflammatory signaling, and age-related epigenetic regulation. These properties make ELOVL2 a useful target for studying metabolic control of membrane dynamics and lipid-dependent signaling in human cells.
ELOVL2 CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous ELOVL2 expression without altering the underlying DNA sequence.
ELOVL2 CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the ELOVL2 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 ELOVL2 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous ELOVL2 expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native ELOVL2 locus and enabling the study of ELOVL2-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of ELOVL2 pathway restoration in tumor cells with silenced or reduced ELOVL2 expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.