ERBIN CRISPR Activation Plasmid (h): sc-402637-ACT

ERBIN (ERBB2 interacting protein) is a PDZ domain–containing scaffold protein that localizes to basolateral membranes and coordinates receptor complex assembly, trafficking, and signal routing. It modulates ERBB2/EGFR pathway output and intersects with MAPK and PI3K signaling by organizing membrane-proximal signaling nodes and coupling receptors to downstream effectors. ERBIN also influences epithelial polarity and junctional organization through interactions with polarity and adhesion regulators, shaping cell architecture and signaling fidelity. Dysregulated ERBIN expression or altered scaffold function has been associated with aberrant growth factor signaling and polarity defects that are relevant to mechanistic studies in oncology and other epithelial pathologies.

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

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

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