Uteroglobin/SCGB1A1/CC10 CRISPR Activation Plasmid (h): sc-400381-ACT

SCGB1A1 encodes uteroglobin (also known as CC10), a secreted member of the secretoglobin family produced primarily by airway club cells and other mucosal epithelia. This small homodimeric protein contributes to epithelial homeostasis by modulating inflammatory signaling, limiting oxidative stress, and influencing phospholipid and eicosanoid metabolism in the airway surface liquid. SCGB1A1 expression is tightly linked to epithelial differentiation programs and is frequently used as a marker of club cell identity and airway remodeling. Altered SCGB1A1 levels have been associated with chronic inflammatory airway conditions and epithelial injury responses, making it relevant for studies of mucosal barrier function and inflammatory regulation.

Uteroglobin/SCGB1A1/CC10 CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous SCGB1A1 expression without altering the underlying DNA sequence.

Uteroglobin/SCGB1A1/CC10 CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the SCGB1A1 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 SCGB1A1 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous Uteroglobin/SCGB1A1/CC10 expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native SCGB1A1 locus and enabling the study of Uteroglobin/SCGB1A1/CC10-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of Uteroglobin/SCGB1A1/CC10 pathway restoration in tumor cells with silenced or reduced SCGB1A1 expression.

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