Aquaporin 1/AQP1 CRISPR Activation Plasmid (m): sc-419172-ACT

Mouse Aqp1 encodes Aquaporin 1 (AQP1), a tetrameric water channel that enables rapid osmotic water movement across plasma membranes and supports fluid homeostasis in microvascular endothelium, renal proximal tubules, and other water-transporting epithelia. By regulating cell volume, transcellular water flux, and local osmotic gradients, AQP1 influences processes such as capillary permeability, epithelial secretion and reabsorption, and migratory behavior in certain cell types. Aqp1-dependent water transport interfaces with pathways controlling ion handling and barrier function, including coordination with solute transporters and tight junction dynamics. Altered AQP1 expression or localization has been linked to dysregulated fluid balance and edema-related phenotypes, making it relevant for studies of kidney physiology, vascular permeability, and tissue fluid microenvironments.

Aquaporin 1/AQP1 CRISPR Activation Plasmid (m) provides a targeted, non-destructive approach to upregulating endogenous Aqp1 expression without altering the underlying DNA sequence.

Aquaporin 1/AQP1 CRISPR Activation Plasmid (m) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the Aqp1 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 Aqp1 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous Aquaporin 1/AQP1 expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native Aqp1 locus and enabling the study of Aquaporin 1/AQP1-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of Aquaporin 1/AQP1 pathway restoration in tumor cells with silenced or reduced Aqp1 expression.

For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.