Pertussis toxin that encode Ptl proteins. Together, these proteins form the PT secretion complex. PT is released from "B. pertussis" in an inactive form. Following PT binding to a cell membrane receptor, it is taken up in an endosome, after which it undergoes retrograde transport to the trans-Golgi network and endoplasmic reticulum. At some point during this transport, the A subunit (or protomer) becomes activated, perhaps through the action of glutathione and ATP. PT catalyzes the ADP-ribosylation of the α subunits of the heterotrimeric G protein. This prevents the G proteins from interacting with G protein-coupled receptors on the cell membrane, thus
Wilson disease protein kidney disease and neurological disease. The major cause is the malfunction of ATP7B by single base pair mutations, deletions, frame-shifts, splice errors in "ATP7B" gene. Wilson disease protein Wilson disease protein (WND), also known as ATP7B protein, is a copper-transporting P-type ATPase which is encoded by the "ATP7B" gene. The ATP7B protein is located in the trans-Golgi network of the liver and brain and balances the copper level in the body by excreting excess copper into bile and plasma. Genetic disorder of the ATP7B gene may cause Wilson's disease, a disease in which copper accumulates in tissues, leading to neurological