Not CRISPR data: the image illustrates antibody quality for visualizing CRISPR experiment results.
Not CRISPR data: the image illustrates antibody quality for visualizing CRISPR experiment results.
VDAC1/Porin CRISPR Activation Plasmid (h2): sc-418200-ACT-2
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- VDAC1/Porin CRISPR Activation Plasmid (h2) is a synergistic activation mediator (SAM) transcription activation system designed to specifically upregulate gene expression
- VDAC1/Porin CRISPR Activation Plasmid (h2) 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 VDAC1/Porin CRISPR Activation Plasmid (h2) and VDAC1/Porin CRISPR Activation Plasmid (h22) target distinct regulatory regions upstream of the VDAC1 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: VDAC1/Porin Antibody (B-6): sc-390996
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
VDAC1/Porin CRISPR Activation Plasmid (h2) | sc-418200-ACT-2 | 20 µg | $397.00 |
Human VDAC1 (voltage-dependent anion-selective channel 1), also known as porin, is a mitochondrial outer membrane channel that governs the exchange of ATP/ADP, metabolites, and ions between mitochondria and cytosol, thereby coordinating cellular bioenergetics and redox homeostasis. It interfaces with hexokinase and BCL-2 family proteins to modulate mitochondrial permeability, calcium handling at mitochondria–ER contact sites, and apoptosis-related processes, linking mitochondrial dynamics to stress signaling. Dysregulated VDAC1 expression or channel activity has been associated with altered metabolic reprogramming and mitochondrial dysfunction observed across cancer, neurodegenerative disorders, and cardiovascular disease contexts. VDAC1-targeted gene editing is commonly applied to dissect mitochondrial transport mechanisms, map protein–protein interaction networks at the outer mitochondrial membrane, and establish causal roles for VDAC1 in cell death susceptibility and metabolic pathway adaptation.
VDAC1/Porin CRISPR Activation Plasmid (h2) provides a targeted, non-destructive approach to upregulating endogenous VDAC1 expression without altering the underlying DNA sequence.
VDAC1/Porin CRISPR Activation Plasmid (h2) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the VDAC1 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 VDAC1 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous VDAC1/Porin expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native VDAC1 locus and enabling the study of VDAC1/Porin-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of VDAC1/Porin pathway restoration in tumor cells with silenced or reduced VDAC1 expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.