MOX-2 CRISPR Activation Plasmid (h): sc-403723-ACT

Human MEOX2 encodes the homeobox transcription factor MOX-2, a nuclear regulator of developmental gene expression programs that influence mesenchymal differentiation, vascular cell behavior, and tissue patterning. MOX-2 integrates into transcriptional networks controlling lineage specification and extracellular matrix remodeling, with reported roles in endothelial and smooth muscle cell biology and context-dependent control of cell cycle and stress-response genes. Altered MEOX2 activity has been associated with vascular dysfunction and aberrant differentiation states, making it relevant for studies of angiogenesis, fibrosis-like remodeling, and developmental dysregulation. As a transcriptional regulator, MOX-2 is commonly investigated using expression profiling and chromatin-based assays to map downstream targets and pathway interactions.

MOX-2 CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous MEOX2 expression without altering the underlying DNA sequence.

MOX-2 CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the MEOX2 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 MEOX2 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous MOX-2 expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native MEOX2 locus and enabling the study of MOX-2-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of MOX-2 pathway restoration in tumor cells with silenced or reduced MEOX2 expression.

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