Androgen Receptor CRISPR Activation Plasmid (m): sc-419181-ACT

Mouse Ar encodes the androgen receptor, a ligand-activated nuclear receptor transcription factor that binds androgens and regulates gene expression programs controlling reproductive development, sexual differentiation, and anabolic metabolism. Upon activation, Androgen Receptor translocates to the nucleus, binds androgen response elements, and integrates with chromatin remodeling and co-regulator complexes to modulate transcriptional networks governing cell proliferation, differentiation, and tissue homeostasis. AR signaling intersects with PI3K/AKT, MAPK, and Wnt/β-catenin pathways, shaping feedback on steroidogenesis and growth-factor responses in multiple organs. Dysregulated AR activity is implicated in endocrine and reproductive phenotypes and provides a mechanistic link to hormone-dependent pathobiology, making Ar a central node for studying transcriptional control by nuclear receptors in vivo and in cell models.

Androgen Receptor CRISPR Activation Plasmid (m) provides a targeted, non-destructive approach to upregulating endogenous Ar expression without altering the underlying DNA sequence.

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

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