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.
Akt1 CRISPR Activation Plasmid (m): sc-419071-ACT
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- Akt1 CRISPR Activation Plasmid (m) is a synergistic activation mediator (SAM) transcription activation system designed to specifically upregulate gene expression
- Akt1 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 Akt1 CRISPR Activation Plasmid (m) and Akt1 CRISPR Activation Plasmid (m2) target distinct regulatory regions upstream of the Akt1 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: Akt1 Antibody (G-5): sc-55523
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
Akt1 CRISPR Activation Plasmid (m) | sc-419071-ACT | 20 µg | $397.00 |
Mouse Akt1 encodes AKT1, a serine/threonine kinase that functions as a central effector of PI3K signaling to coordinate cell survival, glucose metabolism, protein synthesis, and cell-cycle progression. Upon activation downstream of receptor tyrosine kinases and insulin/IGF pathways, AKT1 phosphorylates targets that regulate mTORC1 activity, FOXO transcription factors, and GSK3-dependent processes, shaping anabolic growth and stress responses. Akt1 activity influences cytoskeletal remodeling and migration via cross-talk with MAPK and focal adhesion signaling. Dysregulated AKT1 signaling is broadly implicated in oncogenic growth programs, insulin resistance, and inflammatory phenotypes, making it a key node for pathway interrogation in mouse disease models.
Akt1 CRISPR Activation Plasmid (m) provides a targeted, non-destructive approach to upregulating endogenous Akt1 expression without altering the underlying DNA sequence.
Akt1 CRISPR Activation Plasmid (m) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the Akt1 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 Akt1 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous Akt1 expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native Akt1 locus and enabling the study of Akt1-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of Akt1 pathway restoration in tumor cells with silenced or reduced Akt1 expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.