SMAD3 Reporter Mouse for Assessing TGF- ß/Activin Pathway Activation

This reporter was greater than ten times more sensitive in vitro than the CAGA12-based reporter, another commonly used construct to detect TGF- ß signaling.  Using CRISPR/Cas9 technology, the inventors knocked this reporter construct into the Rosa26 locus, a ubiquitously expressed gene in most cells of the mouse. This strategy allows identification of tissues and cells in which signaling of TGF-βs are endogenously active during normal de velopment, tissue homeostasis, and disease.The mouse model is currently undergoing further validation using genetic and pharmacological approaches. It is available for licensing.Inventors: Caroline Hill () Lalage Wakefield (NCI) Sushil Rane (NIDDH) Yuan Yang (NCI)Commercial Advantages:Development of oncology therapeuticsDeveloping of fibrosis therapeuticsPre-clinicalin vivo model to study TGF- β signaling and pathway antagonistsPre-clinical model for TGF- β/SMAD3 disease statesCompetitive Advantages:No requirement for luciferin injectionsHigher sensitivity for SMAD3 activation than other reporters
Source: NIH OTT Licensing Opportunities - Category: Research Authors: Tags: Research Materials Licensing Desired NCI Source Type: research