Date published: 2026-7-10

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Peg1 CRISPR Activation Plasmid (m): sc-421634-ACT

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Datasheets
  • Target species: mouse
  • 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
  • Peg1 CRISPR Activation Plasmid (m) is a synergistic activation mediator (SAM) transcription activation system designed to specifically upregulate gene expression
  • Peg1 CRISPR Activation Plasmid (m) 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 Peg1 CRISPR Activation Plasmid (m) and Peg1 CRISPR Activation Plasmid (m2) target distinct regulatory regions upstream of the Mest transcriptional start site. One or both designs may be available
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    Ordering Information

    Product NameCatalog #UNITPriceQtyFAVORITES

    Peg1 CRISPR Activation Plasmid (m)

    sc-421634-ACT
    20 µg
    $397.00

    Peg1 CRISPR Activation Plasmid (m2)

    sc-421634-ACT-2
    20 µg
    $397.00

    Mouse Mest encodes the imprinted protein Peg1, a regulator of embryonic growth, placental development, and postnatal metabolic homeostasis. Peg1 has been linked to adipogenesis, energy balance, and cell fate decisions through epigenetic control mechanisms and signaling programs that influence differentiation and tissue remodeling. Altered Mest/Peg1 expression is frequently used as a marker of changes in imprinting status and developmental programming, with relevance to obesity-associated phenotypes and growth dysregulation in model systems. In biomedical research, Mest provides a tractable locus for interrogating how parent-of-origin gene regulation shapes developmental and metabolic pathways.

    Peg1 CRISPR Activation Plasmid (m) provides a targeted, non-destructive approach to upregulating endogenous Mest expression without altering the underlying DNA sequence.

    Peg1 CRISPR Activation Plasmid (m) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the Mest 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 Mest transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous Peg1 expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native Mest locus and enabling the study of Peg1-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of Peg1 pathway restoration in tumor cells with silenced or reduced Mest expression.

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