| Literature DB >> 20176081 |
Abstract
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?" Copyright (c) 2010 Elsevier Ireland Ltd. All rights reserved.Entities:
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Year: 2010 PMID: 20176081 DOI: 10.1016/j.mce.2010.02.020
Source DB: PubMed Journal: Mol Cell Endocrinol ISSN: 0303-7207 Impact factor: 4.102