Future experiments will attempt to determine how such a mutation could also affect pancreatic function. This laboratory has for many years studied human diseases involving trimeric G-proteins. In earlier efforts, the laboratory described the molecular mechanism of cholera, by identifying the G-alpha residue modified by cholera toxin. This modification constitutively activates alpha-s by slowing hydrolysis of GTP, the reaction that turns off G proteins. Replacement of either cyan residue produces an inactive G protein alpha subunit, causing pseudohypoparathyroidism.
Bound nucleotide is light green.