TMPRSS11D CRISPR Activation Plasmid (h): sc-407568-ACT

TMPRSS11D encodes a type II transmembrane serine protease expressed predominantly in epithelial tissues, where it contributes to pericellular proteolysis at the cell surface. By cleaving extracellular or membrane-associated substrates, TMPRSS11D can influence epithelial differentiation, barrier remodeling, and protease-activated signaling pathways that shape inflammatory and tissue homeostatic responses. Dysregulated activity or expression of membrane-anchored serine proteases has been associated with altered mucosal integrity and aberrant remodeling programs observed in chronic airway and upper aerodigestive tract disorders. TMPRSS11D is therefore a useful target for investigating protease-dependent regulation of epithelial microenvironments and context-specific transcriptional programs in human cells.

TMPRSS11D CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous TMPRSS11D expression without altering the underlying DNA sequence.

TMPRSS11D CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the TMPRSS11D 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 TMPRSS11D transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous TMPRSS11D expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native TMPRSS11D locus and enabling the study of TMPRSS11D-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of TMPRSS11D pathway restoration in tumor cells with silenced or reduced TMPRSS11D expression.

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