CEMIP CRISPR Activation Plasmid (h): sc-412779-ACT

CEMIP (cell migration-inducing hyaluronidase 1) encodes a secreted and intracellular hyaluronan-binding protein that modulates extracellular matrix remodeling by promoting hyaluronan depolymerization and turnover. Through regulation of hyaluronan metabolism, CEMIP influences cell adhesion, motility, and stromal interactions, linking matrix dynamics to signaling processes such as EMT-associated programs and inflammatory microenvironment responses. Altered CEMIP expression has been associated with tumor progression, invasion, and metastatic potential across multiple cancer contexts, and it is also implicated in connective tissue and cartilage-related pathophysiology via effects on matrix homeostasis. These properties make CEMIP a useful target for studying ECM-driven regulation of cell behavior, tissue remodeling, and disease-relevant phenotypes in human model systems.

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

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

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