ADRM1 CRISPR Activation Plasmid (h): sc-406903-ACT

ADRM1 (adhesion regulating molecule 1), also known as the proteasomal ubiquitin receptor Rpn13, is a 19S regulatory particle subunit that binds polyubiquitinated substrates and facilitates their delivery to the 26S proteasome for degradation. Through interactions within the ubiquitin–proteasome system, ADRM1 helps maintain proteostasis, modulates turnover of cell-cycle and stress-response regulators, and influences signaling outputs linked to protein quality control. Dysregulated proteasome substrate recognition and altered ADRM1 activity have been associated with changes in cellular viability programs and adaptive responses to proteotoxic stress. As a result, ADRM1 is frequently studied in contexts where ubiquitin-dependent degradation shapes proliferation, DNA damage responses, and inflammation-associated transcriptional programs.

ADRM1 CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous ADRM1 expression without altering the underlying DNA sequence.

ADRM1 CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the ADRM1 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 ADRM1 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous ADRM1 expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native ADRM1 locus and enabling the study of ADRM1-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of ADRM1 pathway restoration in tumor cells with silenced or reduced ADRM1 expression.

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