Cukurova University, Faculty of Medicine, Department of Pediatric Endocrinology and Metabolism, Balcali, Adana 01330, Turkey.
Mol Cell Endocrinol. 2010 Aug 5;324(1-2):64-9. doi: 10.1016/j.mce.2010.02.020. Epub 2010 Feb 20.
Recent reports of humans who have normosmic idiopathic hypogonadotropic hypogonadism due to TAC3 or TACR3 (encoding neurokinin B and its receptor, NK3R, respectively) mutations provided compelling evidence for the involvement of neurokinin B (NKB) signaling in puberty. This apparently stimulated the field to understand the exact mechanism through which NKB signaling exerts its effects. With the important findings from these recent studies a sketch of GnRH pulse generator has emerged in which NKB signaling appears to play a key role. In this communication, NKB involvement in puberty is reviewed from the perspective of the fundamental question of "what controls puberty?"
最近有报道称,由于 TAC3 或 TACR3(分别编码神经激肽 B 和其受体 NK3R)突变,人类出现了正常嗅觉的特发性低促性腺激素性性腺功能减退症,这为神经激肽 B(NKB)信号在青春期中的作用提供了有力证据。这显然激发了该领域的研究人员去深入了解 NKB 信号发挥作用的确切机制。随着这些最新研究的重要发现,一个 GnRH 脉冲发生器的草图已经出现,其中 NKB 信号似乎起着关键作用。在本通讯中,从“什么控制青春期?”这一基本问题的角度来综述 NKB 参与青春期的相关内容。