ADAMDEC1 CRISPR Activation Plasmid (h): sc-405515-ACT

ADAMDEC1 encodes a secreted metalloprotease of the ADAM (a disintegrin and metalloprotease) family that contributes to extracellular matrix remodeling and regulation of pericellular proteolysis. It is predominantly associated with myeloid and mucosal immune compartments, where it has been linked to inflammatory signaling, leukocyte differentiation, and tissue surveillance processes. Through modulation of the extracellular milieu, ADAMDEC1 can influence cell migration, adhesion dynamics, and cytokine-responsive pathways that shape local immune responses. Altered ADAMDEC1 expression has been reported in studies of gastrointestinal inflammation, tumor microenvironment biology, and immune infiltration, supporting its value as a molecular readout in immunology and cancer research.

ADAMDEC1 CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous ADAMDEC1 expression without altering the underlying DNA sequence.

ADAMDEC1 CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the ADAMDEC1 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 ADAMDEC1 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous ADAMDEC1 expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native ADAMDEC1 locus and enabling the study of ADAMDEC1-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of ADAMDEC1 pathway restoration in tumor cells with silenced or reduced ADAMDEC1 expression.

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