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.
ACAP1 CRISPR Activation Plasmid (h): sc-405104-ACT
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- ACAP1 CRISPR Activation Plasmid (h) is a synergistic activation mediator (SAM) transcription activation system designed to specifically upregulate gene expression
- ACAP1 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 ACAP1 CRISPR Activation Plasmid (h) and ACAP1 CRISPR Activation Plasmid (h2) target distinct regulatory regions upstream of the ACAP1 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: ACAP1 Antibody (B-11): sc-376574
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
ACAP1 CRISPR Activation Plasmid (h) | sc-405104-ACT | 20 µg | $397.00 |
ACAP1 (ArfGAP with coiled-coil, ankyrin repeat and PH domains 1) encodes an ARF6-regulated GTPase-activating protein that couples phosphoinositide binding to membrane trafficking events. ACAP1 functions in clathrin-associated endocytic recycling, helping control cargo sorting and return of receptors and adhesion molecules to the plasma membrane, thereby influencing cell polarity, migration, and signaling dynamics. Through its roles in recycling endosomes and actin-linked trafficking, ACAP1 is relevant to pathways governing receptor turnover, integrin-dependent adhesion, and immune cell membrane remodeling. Dysregulated endosomal recycling and ARF6 network activity have been implicated in oncogenic signaling, invasion-associated phenotypes, and immune dysfunction, making ACAP1 a useful node for mechanistic studies of trafficking-dependent regulation.
ACAP1 CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous ACAP1 expression without altering the underlying DNA sequence.
ACAP1 CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the ACAP1 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 ACAP1 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous ACAP1 expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native ACAP1 locus and enabling the study of ACAP1-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of ACAP1 pathway restoration in tumor cells with silenced or reduced ACAP1 expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.