Date published: 2026-7-10

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Bax CRISPR Activation Plasmid (h): sc-400042-ACT

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Datasheets
  • Target species: human
  • 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
  • Bax CRISPR Activation Plasmid (h) is a synergistic activation mediator (SAM) transcription activation system designed to specifically upregulate gene expression
  • Bax 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 Bax CRISPR Activation Plasmid (h) and Bax CRISPR Activation Plasmid (h2) target distinct regulatory regions upstream of the BAX 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: Bax Antibody (B-9): sc-7480
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    Ordering Information

    Product NameCatalog #UNITPriceQtyFAVORITES

    Bax CRISPR Activation Plasmid (h)

    sc-400042-ACT
    20 µg
    $397.00

    Human BAX encodes Bax, a pro-apoptotic BCL-2 family effector that governs mitochondrial outer membrane permeabilization and cytochrome c release, initiating caspase activation and intrinsic apoptosis. Bax activity is regulated by BH3-only proteins and counterbalanced by anti-apoptotic BCL-2 members, integrating cellular stress signals such as DNA damage and growth factor deprivation. This pathway intersects with p53-dependent stress responses, mitochondrial dynamics, and proteostasis to shape cell fate decisions. Dysregulated BAX expression or signaling contributes to altered apoptosis thresholds observed across cancer biology, neurodegeneration, and immune homeostasis, making BAX a key node for mechanistic studies of cell death control.

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

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

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