
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
ARAP3 CRISPR Activation Plasmid (h) | sc-405365-ACT | 20 µg | $397.00 |
ARAP3 (also known as CENTD3) encodes a phosphoinositide-binding ArfGAP and RhoGAP that couples PI3K signaling to coordinated regulation of ARF6- and Rho-family GTPases. Through its multi-domain architecture, ARAP3 modulates actin cytoskeletal remodeling, membrane trafficking, integrin-dependent adhesion, and chemotactic responses, particularly in endothelial and hematopoietic lineages. ARAP3 activity interfaces with pathways governing cell migration, vascular morphogenesis, and inflammatory signaling, making it relevant to studies of angiogenesis and leukocyte trafficking. Dysregulated small-GTPase signaling and altered ARAP3 expression have been associated with cancer cell invasion and tumor microenvironment remodeling, supporting its use as a node for mechanistic pathway interrogation.
ARAP3 CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous ARAP3 expression without altering the underlying DNA sequence.
ARAP3 CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the ARAP3 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 ARAP3 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous ARAP3 expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native ARAP3 locus and enabling the study of ARAP3-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of ARAP3 pathway restoration in tumor cells with silenced or reduced ARAP3 expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.