Legros J J, Geenen V
Endocrinology Department, Centre Hospitalier Universitaire-Sart Tilman, Liège, Belgium.
Horm Res. 1996;45(3-5):182-6. doi: 10.1159/000184784.
When they were discovered by Acher and co-workers, neurophysins were thought to act as carriers for the active nonapeptides vasopressin (AVP) and oxytocin (OT) and were then recognized as the inactive fragment of a precursor with a higher molecular weight (propressophysin). The role of neurophysins in the hypothalamo-neurohypophyseal system is now being reconsidered in the light of crystallographic and molecular biology research and the recent definition of the different deletions or substitutions that cause central diabetes insipidus in rats (Brattleboro) or human beings. Apparently, any disruption of the structure and/or conformation of neurophysins (by genic substitution or deletion) may cause a decline in the binding and the activity of the endopeptidase responsible for the cleavage of the AVP. The disruption may also produce a change in the polymerization of neurophysins and salt bridges relating this to the neuropeptides, with the result that there is an accelerated aspecific enzymatic degradation of the hormone revealing clinical symptomatology. So, rather than being a mere inactive part of the precursor, neurophysins are now equally regarded as a system for carrying and protecting nonapeptides.
当神经垂体素被阿彻及其同事发现时，它们被认为是活性九肽血管加压素（AVP）和催产素（OT）的载体，随后被确认为一种分子量更高的前体（加压素原）的无活性片段。鉴于晶体学和分子生物学研究以及最近对导致大鼠（布拉特洛维）或人类中枢性尿崩症的不同缺失或替代的定义，神经垂体素在下丘脑 - 神经垂体系统中的作用现在正在重新考虑。显然，神经垂体素的结构和/或构象的任何破坏（通过基因替代或缺失）可能导致负责AVP裂解的内肽酶的结合和活性下降。这种破坏还可能导致神经垂体素的聚合以及与神经肽相关的盐桥发生变化，结果是激素的非特异性酶促降解加速，从而揭示临床症状。因此，神经垂体素现在不再仅仅被视为前体的无活性部分，而是同样被视为一种携带和保护九肽的系统。
