GIPC2 CRISPR Activation Plasmid (h): sc-405087-ACT

GIPC2 (GAIP-interacting protein, C terminus 2) is a PDZ domain–containing adaptor implicated in organizing membrane-associated signaling complexes and coordinating receptor trafficking. Through PDZ-mediated protein–protein interactions, GIPC2 can influence endocytic sorting, vesicular transport, and downstream signal propagation that shape cell polarity, migration, and growth-control programs. Altered expression patterns of GIPC family adaptors have been linked to dysregulated signaling circuits in cancer biology and other disorders involving aberrant receptor turnover, supporting investigation of GIPC2 in context-dependent transcriptional and phenotypic states. Studying GIPC2 regulation helps clarify how scaffold proteins couple surface receptor dynamics to intracellular pathways that govern cellular behavior.

GIPC2 CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous GIPC2 expression without altering the underlying DNA sequence.

GIPC2 CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the GIPC2 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 GIPC2 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous GIPC2 expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native GIPC2 locus and enabling the study of GIPC2-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of GIPC2 pathway restoration in tumor cells with silenced or reduced GIPC2 expression.

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