Date published: 2026-7-14

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FPR CRISPR Activation Plasmid (h): sc-418173-ACT

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Datasheets
  • Target species: human
  • 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
  • FPR CRISPR Activation Plasmid (h) is a synergistic activation mediator (SAM) transcription activation system designed to specifically upregulate gene expression
  • FPR 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 FPR CRISPR Activation Plasmid (h) and FPR CRISPR Activation Plasmid (h2) target distinct regulatory regions upstream of the FPR1 transcriptional start site. One or both designs may be available
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    Ordering Information

    Product NameCatalog #UNITPriceQtyFAVORITES

    FPR CRISPR Activation Plasmid (h)

    sc-418173-ACT
    20 µg
    $397.00

    Formyl peptide receptor 1 (FPR1) encodes FPR, a seven-transmembrane GPCR that detects N-formylated peptides derived from bacteria and damaged mitochondria, enabling rapid neutrophil and monocyte chemotaxis. FPR1 couples primarily to Gi proteins to activate PLCβ, intracellular Ca2+ flux, PI3K/AKT, and MAPK signaling, coordinating actin remodeling, integrin activation, degranulation, and reactive oxygen species generation. Through these pathways, FPR1 shapes innate immune surveillance and the inflammatory microenvironment at sites of infection or sterile tissue injury. Dysregulated FPR1 signaling has been investigated in chronic inflammatory conditions and tumor-associated inflammation, where altered leukocyte recruitment and activation can influence disease biology.

    FPR CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous FPR1 expression without altering the underlying DNA sequence.

    FPR CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the FPR1 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 FPR1 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous FPR expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native FPR1 locus and enabling the study of FPR-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of FPR pathway restoration in tumor cells with silenced or reduced FPR1 expression.

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