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.
ARF6 CRISPR Activation Plasmid (h): sc-400799-ACT
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- ARF6 CRISPR Activation Plasmid (h) is a synergistic activation mediator (SAM) transcription activation system designed to specifically upregulate gene expression
- ARF6 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 ARF6 CRISPR Activation Plasmid (h) and ARF6 CRISPR Activation Plasmid (h2) target distinct regulatory regions upstream of the ARF6 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: ARF6 Antibody (3A-1): sc-7971
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
ARF6 CRISPR Activation Plasmid (h) | sc-400799-ACT | 20 µg | $397.00 |
ARF6 encodes a small Ras-related GTPase that regulates plasma membrane remodeling, clathrin-independent endocytosis, and recycling of membrane proteins through coordinated control of phosphoinositide metabolism and actin dynamics. Cycling between GDP- and GTP-bound states positions ARF6 as an upstream regulator of pathways governing cell polarity, adherens junction turnover, and integrin trafficking, thereby influencing migration and invasive behavior. ARF6 signaling interfaces with RHO family GTPases and MAPK/PI3K-associated programs that tune cytoskeletal organization and receptor availability at the cell surface. Dysregulated ARF6 activity has been linked to altered motility and metastasis-associated phenotypes in cancer models and to defects in neuronal morphogenesis and synaptic membrane trafficking relevant to neurobiology.
ARF6 CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous ARF6 expression without altering the underlying DNA sequence.
ARF6 CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the ARF6 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 ARF6 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous ARF6 expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native ARF6 locus and enabling the study of ARF6-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of ARF6 pathway restoration in tumor cells with silenced or reduced ARF6 expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.