Date published: 2026-7-10

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EAF1 CRISPR Activation Plasmid (m): sc-428881-ACT

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Datasheets
  • Target species: mouse
  • 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
  • EAF1 CRISPR Activation Plasmid (m) is a synergistic activation mediator (SAM) transcription activation system designed to specifically upregulate gene expression
  • EAF1 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 EAF1 CRISPR Activation Plasmid (m) and EAF1 CRISPR Activation Plasmid (m2) target distinct regulatory regions upstream of the Eaf1 transcriptional start site. One or both designs may be available
  • Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: EAF1 Antibody (A-10): sc-373832
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    Ordering Information

    Product NameCatalog #UNITPriceQtyFAVORITES

    EAF1 CRISPR Activation Plasmid (m)

    sc-428881-ACT
    20 µg
    $397.00

    Mouse Eaf1 encodes EAF1, a nuclear transcriptional cofactor originally characterized as an ELL-associated factor that helps coordinate RNA polymerase II elongation and gene expression programs. EAF1 participates in chromatin-associated regulatory complexes and has been linked to control of cell cycle progression, differentiation, and stress-responsive transcriptional outputs. Through its role in transcriptional regulation, EAF1 can influence pathways governing proliferation and developmental gene networks, making it relevant to studies of dysregulated transcription in cancer biology and other contexts where gene expression control is perturbed. Investigating Eaf1 function supports mechanistic dissection of transcriptional elongation and promoter-proximal regulatory events in mammalian cells.

    EAF1 CRISPR Activation Plasmid (m) provides a targeted, non-destructive approach to upregulating endogenous Eaf1 expression without altering the underlying DNA sequence.

    EAF1 CRISPR Activation Plasmid (m) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the Eaf1 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 Eaf1 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous EAF1 expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native Eaf1 locus and enabling the study of EAF1-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of EAF1 pathway restoration in tumor cells with silenced or reduced Eaf1 expression.

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