
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
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.