Role of the enigmatic TRα2 isoform in regulating cardiac TH function

Prof. Dr. Frank Kaiser

TH action in the heart is predominantly controlled by its receptor TRα1, but a non-hormone binding TRα2 splice-variant is dynamically produced from the same mRNA under pathological conditions such as heart failure. In the proposed project, we aim to test the hypothesis that this TRα2 isoform modulates local thyroid hormone action in the heart. We will employ iPSC-derived heart model systems with tagged TRs for chromatin- and protein-protein interactions and characterise the consequences of TRα2 mutations for these functions.