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
Schindler disease of the disease is mostly palliative. However, Type II Schindler disease, with its late onset of symptoms, is not characterized by neurological degeneration. There is no known cure for Schindler disease, but bone marrow transplants have been trialed, as they have been successful in curing other glycoprotein disorders. Schindler disease was named after Detlev Schindler (1946- ) M.D., the first author of a 1988 paper detailing the disease. It also named after the Japanese Biochemist and Physician, Hiro Kanzaki (1949- ), who further studied it and released papers detailing the disease in 2006. Schindler disease Schindler disease, also known as