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.
beta Actin CRISPR Activation Plasmid (h2): sc-400000-ACT-2
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- beta Actin CRISPR Activation Plasmid (h2) is a synergistic activation mediator (SAM) transcription activation system designed to specifically upregulate gene expression
- beta Actin 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 beta Actin CRISPR Activation Plasmid (h2) and beta Actin CRISPR Activation Plasmid (h22) target distinct regulatory regions upstream of the ACTB 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: beta Actin Antibody (C4): sc-47778
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
beta Actin CRISPR Activation Plasmid (h2) | sc-400000-ACT-2 | 20 µg | $397.00 |
Human ACTB encodes beta-actin, a highly conserved cytoskeletal protein that polymerizes into microfilaments to drive cell shape maintenance, polarity, contractility, and motility. Beta-actin dynamics are central to actin cytoskeleton remodeling pathways that coordinate focal adhesion turnover, mechanotransduction, cytokinesis, and vesicle trafficking, and they contribute to transcriptional regulation through actin-dependent nuclear processes. Perturbation of ACTB or its interacting networks is linked to developmental disorders and altered cytoskeletal organization observed in cancer cell invasion and metastasis, underscoring its value for studying genotype–phenotype relationships. ACTB-targeted gene editing and functional genomics workflows are commonly used to interrogate actin-regulated signaling, quantify cytoskeletal phenotypes in live-cell imaging, and establish robust reference contexts for pathway perturbation studies.
beta Actin CRISPR Activation Plasmid (h2) provides a targeted, non-destructive approach to upregulating endogenous ACTB expression without altering the underlying DNA sequence.
beta Actin CRISPR Activation Plasmid (h2) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the ACTB 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 ACTB transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous beta Actin expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native ACTB locus and enabling the study of beta Actin-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of beta Actin pathway restoration in tumor cells with silenced or reduced ACTB expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.