RXRβ CRISPR Activation Plasmid (h): sc-402266-ACT

Retinoid X receptor beta (RXRB; RXRβ) is a ligand-activated nuclear receptor that functions as a core transcriptional partner for multiple receptor families, including PPARs, LXRs, FXR, VDR, and thyroid hormone receptors. By forming heterodimers and binding retinoid response elements, RXRβ coordinates gene programs controlling lipid and glucose metabolism, cholesterol and bile acid homeostasis, inflammation, and cellular differentiation. RXRB-dependent transcriptional regulation integrates retinoid signaling with broader nuclear receptor networks that shape tissue-specific metabolic and immune states. Dysregulated RXRβ signaling has been implicated in metabolic disorders and cancer-related transcriptional rewiring, making RXRB a useful node for pathway-focused mechanistic studies.

RXRβ CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous RXRB expression without altering the underlying DNA sequence.

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

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