DIP2C CRISPR Activation Plasmid (h): sc-411642-ACT

Human DIP2C (disco-interacting protein 2 homolog C) is a nuclear-associated protein implicated in chromatin-linked regulation of gene expression and maintenance of cellular identity programs. Reported functions connect DIP2 family members to epigenetic control, DNA methylation-associated processes, and differentiation-related transcriptional networks that shape proliferation and lineage commitment. Altered DIP2C expression and copy-number changes have been observed in multiple tumor contexts, supporting its relevance to dysregulated transcriptional states and genome-wide regulatory remodeling. These features make DIP2C a useful target for studying transcriptional control, cell state transitions, and cancer-relevant regulatory circuitry in human cells.

DIP2C CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous DIP2C expression without altering the underlying DNA sequence.

DIP2C CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the DIP2C 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 DIP2C transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous DIP2C expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native DIP2C locus and enabling the study of DIP2C-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of DIP2C pathway restoration in tumor cells with silenced or reduced DIP2C expression.

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