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- W2474964516 abstract "a b s t r a c t The paradigm saying that release of the brain neuropeptide big prothoracicotropic hormone (PTTH) ini- tiates metamorphosis by activating the Torso-receptor/ERK pathway in larval prothoracic glands (PGs) is widely accepted nowadays. Upon ligand-receptor interaction Ca2+ enters the PG cells and acts as a secondary messenger. Ecdysteroidogenesis results, later followed by apoptosis. Yet, some data do not fit in this model. In some species decapitated animals can still molt, even repeatedly, and metamor- phose. PTTH does not universally occur in all insect species. PGs may also have other functions; PGs as counterpart of the vertebrate thymus? There are also small PTTHs. Finally, PTTH remains abundantly present in adults and plays a role in control of ecdysteroidogenesis (=sex steroid production) in gonads. This is currently documented only in males. This urges a rethinking of the PTTH-PG paradigm. The key question is: Why does PTTH-induced Ca2+ entry only result in ecdysteroidogenesis and apoptosis in specific cells/tissues, namely the PGs and gonads? Indeed, numerous other neuropeptides also use Ca2+ as secondary messenger. The recent rediscovery that in both invertebrates and vertebrates at least some isoforms of Ca" @default.
- W2474964516 created "2016-07-22" @default.
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- W2474964516 date "2014-01-01" @default.
- W2474964516 modified "2023-09-27" @default.
- W2474964516 title "Initiation of metamorphosis and control of ecdysteroid biosynthesis in insects: The interplay of absence of Juvenile hormone, PTTH, and" @default.
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