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.
SIRT3 CRISPR Activation Plasmid (h): sc-400675-ACT
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- SIRT3 CRISPR Activation Plasmid (h) is a synergistic activation mediator (SAM) transcription activation system designed to specifically upregulate gene expression
- SIRT3 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 SIRT3 CRISPR Activation Plasmid (h) and SIRT3 CRISPR Activation Plasmid (h2) target distinct regulatory regions upstream of the SIRT3 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: SIRT3 Antibody (F-10): sc-365175
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
SIRT3 CRISPR Activation Plasmid (h) | sc-400675-ACT | 20 µg | $397.00 | |||
SIRT3 CRISPR Activation Plasmid (h2) | sc-400675-ACT-2 | 20 µg | $397.00 |
Human SIRT3 encodes a mitochondrial NAD+-dependent deacetylase that regulates protein acetylation to coordinate oxidative metabolism, mitochondrial biogenesis, and redox homeostasis. By deacetylating targets involved in fatty acid oxidation, the TCA cycle, and electron transport chain function, SIRT3 influences ATP production, ROS detoxification, and mitochondrial quality control pathways such as mitophagy. SIRT3 activity links nutrient sensing and stress responses to cellular survival programs, with downstream effects on AMPK/PGC-1α signaling and antioxidant defenses including SOD2-dependent ROS buffering. Dysregulated SIRT3 expression or activity has been associated with mitochondrial dysfunction phenotypes relevant to metabolic disease biology, neurodegeneration research, and cancer metabolism studies.
SIRT3 CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous SIRT3 expression without altering the underlying DNA sequence.
SIRT3 CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the SIRT3 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 SIRT3 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous SIRT3 expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native SIRT3 locus and enabling the study of SIRT3-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of SIRT3 pathway restoration in tumor cells with silenced or reduced SIRT3 expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.