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Title: Critical roles of nardilysin in the maintenance of body temperature homoeostasis.
Authors: Hiraoka, Yoshinori
Matsuoka, Tatsuhiko
Ohno, Mikiko  kyouindb  KAKEN_id
Nakamura, Kazuhiro  KAKEN_id
Saijo, Sayaka
Matsumura, Shigenobu  kyouindb  KAKEN_id
Nishi, Kiyoto
Sakamoto, Jiro
Chen, Po-Min
Inoue, Kazuo  kyouindb  KAKEN_id  orcid (unconfirmed)
Fushiki, Tohru
Kita, Toru
Kimura, Takeshi  kyouindb  KAKEN_id
Nishi, Eiichiro  kyouindb  KAKEN_id
Author's alias: 西, 英一郎
Keywords: Biological sciences
Medical research
Issue Date: 4-Feb-2014
Publisher: Nature Publishing Group
Journal title: Nature communications
Volume: 5
Thesis number: 3224
Abstract: Body temperature homoeostasis in mammals is governed centrally through the regulation of shivering and non-shivering thermogenesis and cutaneous vasomotion. Non-shivering thermogenesis in brown adipose tissue (BAT) is mediated by sympathetic activation, followed by PGC-1α induction, which drives UCP1. Here we identify nardilysin (Nrd1 and NRDc) as a critical regulator of body temperature homoeostasis. Nrd1(-/-) mice show increased energy expenditure owing to enhanced BAT thermogenesis and hyperactivity. Despite these findings, Nrd1(-/-) mice show hypothermia and cold intolerance that are attributed to the lowered set point of body temperature, poor insulation and impaired cold-induced thermogenesis. Induction of β3-adrenergic receptor, PGC-1α and UCP1 in response to cold is severely impaired in the absence of NRDc. At the molecular level, NRDc and PGC-1α interact and co-localize at the UCP1 enhancer, where NRDc represses PGC-1α activity. These findings reveal a novel nuclear function of NRDc and provide important insights into the mechanism of thermoregulation.
Description: 「体温恒常性維持のメカニズムの解明」に成功. 京都大学プレスリリース. 2014-02-04.
Rights: © 2014 Macmillan Publishers Limited.
This work is licensed under a Creative Commons Attribution-NonCommercial-NoDerivs 3.0 Unported License. To view a copy of this license, visit
DOI(Published Version): 10.1038/ncomms4224
PubMed ID: 24492630
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