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.
Akt2 CRISPR Activation Plasmid (m): sc-419072-ACT
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- Akt2 CRISPR Activation Plasmid (m) is a synergistic activation mediator (SAM) transcription activation system designed to specifically upregulate gene expression
- Akt2 CRISPR Activation Plasmid (m) 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 Akt2 CRISPR Activation Plasmid (m) and Akt2 CRISPR Activation Plasmid (m2) target distinct regulatory regions upstream of the Akt2 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: Akt2 Antibody (1G8C12): sc-81148
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
Akt2 CRISPR Activation Plasmid (m) | sc-419072-ACT | 20 µg | $397.00 | |||
Akt2 CRISPR Activation Plasmid (m2) | sc-419072-ACT-2 | 20 µg | $397.00 |
Mouse Akt2 encodes AKT serine/threonine kinase 2, a central effector of PI3K signaling that couples insulin and growth factor receptor inputs to cellular metabolism, survival, and growth. AKT2 regulates GLUT4 trafficking and glucose uptake, glycogen synthesis via GSK3 inhibition, and mTORC1-mediated protein synthesis, while also influencing FOXO-dependent transcription and apoptotic pathways. In metabolic tissues, Akt2 activity shapes adipogenesis and hepatic gluconeogenic programs, and altered signaling is widely used to model insulin resistance and diabetes-relevant phenotypes. In addition, dysregulated AKT2 signaling intersects with oncogenic PI3K–AKT–mTOR networks that impact proliferation, migration, and stress adaptation in diverse experimental systems.
Akt2 CRISPR Activation Plasmid (m) provides a targeted, non-destructive approach to upregulating endogenous Akt2 expression without altering the underlying DNA sequence.
Akt2 CRISPR Activation Plasmid (m) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the Akt2 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 Akt2 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous Akt2 expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native Akt2 locus and enabling the study of Akt2-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of Akt2 pathway restoration in tumor cells with silenced or reduced Akt2 expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.