Open access
Aug 2026
The ZBTB16/CUL3/ROC1 ubiquitin ligase drives the degradation of pathogenic pendrin (SLC26A4) protein variants
A primary mechanism of SLC26A4 regulation in the inner ear and kidney and of SLC26A4 loss of function in Pendred syndrome and deafness DFNB4 is described and a atomistic model of the complete SLC26A4/ZBTB16/Cullin 3/RocI complex is provided in agreement with experimental results.
Florian Huber, E. Bernardinelli, Bassam G. Haddad et al.
· Journal of Biomedical Scienc... · 0 citations