Pertussis toxin interfering with intracellular communication. The Gi subunits remain locked in their GDP-bound, inactive state, thus unable to inhibit adenylate cyclase activity, leading to increased cellular concentrations of cAMP. Increased intracellular cAMP affects normal biological signaling. The toxin causes several systemic effects, among which is an increased release of insulin, causing hypoglycemia. Whether the effects of pertussis toxin are responsible for the paroxysmal cough remains unknown. As a result of this unique mechanism, PT has also become widely used as a biochemical tool to ADP-ribosylate GTP-binding proteins in the study of signal transduction. It has also become an essential component of
Vogt–Koyanagi–Harada disease at the University of Tokyo, in 1911. It was the much later article, published in 1929, that definitively associated Koyanagi with the disease. Harada's 1926 paper is recognized for its comprehensive description of what is now known as Vogt–Koyanagi–Harada disease. Vogt–Koyanagi–Harada disease Vogt–Koyanagi–Harada disease (VKH), also known as Vogt–Koyanagi–Harada syndrome, uveomeningitis syndrome and uveomeningoencephalitic syndrome, is a multisystem disease of presumed autoimmune cause, that affects pigmented tissues, which have melanin. The most significant manifestation is bilateral, diffuse uveitis, which affects the eye. VKH may variably also involve the inner ear with effects on hearing, the skin, and the meninges of