Date published: 2026-7-14

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ACSVL5 CRISPR Activation Plasmid (h): sc-401578-ACT

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Datasheets
  • Target species: human
  • 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
  • ACSVL5 CRISPR Activation Plasmid (h) is a synergistic activation mediator (SAM) transcription activation system designed to specifically upregulate gene expression
  • ACSVL5 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 ACSVL5 CRISPR Activation Plasmid (h) and ACSVL5 CRISPR Activation Plasmid (h2) target distinct regulatory regions upstream of the SLC27A1 transcriptional start site. One or both designs may be available
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    Ordering Information

    Product NameCatalog #UNITPriceQtyFAVORITES

    ACSVL5 CRISPR Activation Plasmid (h)

    sc-401578-ACT
    20 µg
    $397.00

    Human SLC27A1 encodes ACSVL5 (FATP1), a long-chain acyl-CoA synthetase that catalyzes ATP-dependent activation of long-chain fatty acids to acyl-CoA, coupling lipid uptake to intracellular metabolic utilization. By directing fatty acids into β-oxidation, triglyceride and phospholipid biosynthesis, and lipid droplet dynamics, ACSVL5 helps shape cellular energy balance and membrane remodeling. SLC27A1 activity interfaces with PPAR-regulated lipid programs and influences mitochondrial and ER lipid flux, linking nutrient availability to metabolic signaling. Dysregulated fatty acid handling involving SLC27A1 has been associated with metabolic phenotypes and lipid-driven cellular stress pathways, making it relevant to studies of insulin sensitivity, inflammation, and metabolic reprogramming in disease models.

    ACSVL5 CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous SLC27A1 expression without altering the underlying DNA sequence.

    ACSVL5 CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the SLC27A1 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 SLC27A1 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous ACSVL5 expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native SLC27A1 locus and enabling the study of ACSVL5-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of ACSVL5 pathway restoration in tumor cells with silenced or reduced SLC27A1 expression.

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