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.
COX4 CRISPR Activation Plasmid (h): sc-400616-ACT
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- COX4 CRISPR Activation Plasmid (h) is a synergistic activation mediator (SAM) transcription activation system designed to specifically upregulate gene expression
- COX4 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 COX4 CRISPR Activation Plasmid (h) and COX4 CRISPR Activation Plasmid (h2) target distinct regulatory regions upstream of the COX4I1 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: COX4 Antibody (F-8): sc-376731
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
COX4 CRISPR Activation Plasmid (h) | sc-400616-ACT | 20 µg | $397.00 | |||
COX4 CRISPR Activation Plasmid (h2) | sc-400616-ACT-2 | 20 µg | $397.00 |
Human COX4I1 encodes cytochrome c oxidase subunit IV isoform 1 (COX4), a nuclear-encoded structural component of mitochondrial complex IV that helps regulate electron transfer from cytochrome c to molecular oxygen and supports oxidative phosphorylation. By influencing complex IV activity, COX4 contributes to mitochondrial membrane potential maintenance, ATP production, and reactive oxygen species homeostasis, integrating into broader bioenergetic and stress-response programs. COX4I1 expression and complex IV stoichiometry are frequently evaluated in studies of mitochondrial dysfunction, hypoxia adaptation, and metabolic reprogramming that accompany proliferative and degenerative disease states. As a core marker of respiratory chain integrity, COX4 is commonly used to connect changes in mitochondrial biogenesis and proteostasis with altered cellular metabolism.
COX4 CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous COX4I1 expression without altering the underlying DNA sequence.
COX4 CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the COX4I1 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 COX4I1 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous COX4 expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native COX4I1 locus and enabling the study of COX4-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of COX4 pathway restoration in tumor cells with silenced or reduced COX4I1 expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.