EDIL3 CRISPR Activation Plasmid (h): sc-404813-ACT

EDIL3 (EGF-like repeats and discoidin I-like domains 3), also known as DEL-1, encodes a secreted extracellular matrix-associated glycoprotein that modulates cell adhesion, migration, and tissue remodeling through integrin-dependent interactions. In human cells, EDIL3 participates in regulation of endothelial behavior and extracellular signaling cues that shape angiogenic and inflammatory microenvironments, influencing leukocyte–endothelium dynamics and matrix organization. Dysregulated EDIL3 expression has been reported in contexts of vascular remodeling and tumor-associated stroma, supporting its relevance for studies of angiogenesis, immune regulation, and metastatic niche biology. These properties make EDIL3 a useful target for dissecting extracellular matrix signaling, integrin pathway crosstalk, and microenvironment-driven phenotypes.

EDIL3 CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous EDIL3 expression without altering the underlying DNA sequence.

EDIL3 CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the EDIL3 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 EDIL3 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous EDIL3 expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native EDIL3 locus and enabling the study of EDIL3-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of EDIL3 pathway restoration in tumor cells with silenced or reduced EDIL3 expression.

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