The Quitterer Group has published their new research findings on BBLN, CAMK2D and Tetralogy of Fallot (TOF) in the journal Nature Cardiovascular Research.
Our group has presented new knowledge about the function of the orphan protein BBLN, revealing the activation of the enzyme CAMK2D by BBLN. Increased BBLN activity stimulated CAMK2D activity, promoting heart fibrosis and causing heart failure in mice with cardiac pressure overload. The newly identified mechanism has relevance for children suffering from the severe heart defect tetralogy of Fallot (TOF).
The abstract of this finding and the complete article can be found in "external pageNature Cardiovascular Research":
external pagehttps://www.nature.com/articles/s44161-023-00351-6