Structural Basis for Specificity of TGFbeta Family Receptor Small Molecule Inhibitors
Ogunjimi, A.A., Zeqiraj, E., Ceccarelli, D.F., Sicheri, F., Wrana, J.L., David, L.(2012) Cell Signal 24: 476-483
- PubMed: 21983015 
- DOI: https://doi.org/10.1016/j.cellsig.2011.09.027
- Primary Citation of Related Structures:  
3TZM - PubMed Abstract: 
Transforming growth factor-¦Â (TGF¦Â) receptor kinase inhibitors have a great therapeutic potential. SB431542 is one of the mainly used kinase inhibitors of the TGF¦Â/Activin pathway receptors, but needs improvement of its EC(50) (EC(50)=1 ¦ÌM) to be translated to clinical use. A key feature of SB431542 is that it specifically targets receptors from the TGF¦Â/Activin pathway but not the closely related receptors from the bone morphogenic proteins (BMP) pathway. To understand the mechanisms of this selectivity, we solved the crystal structure of the TGF¦Â type I receptor (T¦ÂRI) kinase domain in complex with SB431542. We mutated T¦ÂRI residues coordinating SB431542 to their counterparts in activin-receptor like kinase 2 (ALK2), a BMP receptor kinase, and tested the kinase activity of mutated T¦ÂRI. We discovered that a Ser280Thr mutation yielded a T¦ÂRI variant that was resistant to SB431542 inhibition. Furthermore, the corresponding Thr283Ser mutation in ALK2 yielded a BMP receptor sensitive to SB431542. This demonstrated that Ser280 is the key determinant of selectivity for SB431542. This work provides a framework for optimising the SB431542 scaffold to more potent and selective inhibitors of the TGF¦Â/Activin pathway.
Organizational Affiliation: 
Center for Systems Biology, Samuel Lunenfeld Research Institute, Mount Sinai Hospital, 600 University Avenue, Toronto, Ontario, Canada M5G 1X5.