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Title: Anti–USAG-1 therapy for tooth regeneration through enhanced BMP signaling
Authors: Murashima-Suginami, A.
Kiso, H.
Tokita, Y.
Mihara, E.
Nambu, Y.
Uozumi, R.
Tabata, Y.
Bessho, K.
Takagi, J.
Sugai, M.
Takahashi, K.
Author's alias: 村島-杉並, 亜希子
喜早, ほのか
時田, 義人
三原, 恵美子
南部, 由希子
魚住, 龍史
田畑, 泰彦
別所, 和久
高木, 淳一
菅井, 学
高橋, 克
Issue Date: 10-Feb-2021
Publisher: American Association for the Advancement of Science (AAAS)
Journal title: Science Advances
Volume: 7
Issue: 7
Thesis number: eabf1798
Abstract: Uterine sensitization–associated gene-1 (USAG-1) deficiency leads to enhanced bone morphogenetic protein (BMP) signaling, leading to supernumerary teeth formation. Furthermore, antibodies interfering with binding of USAG-1 to BMP, but not lipoprotein receptor–related protein 5/6 (LRP5/6), accelerate tooth development. Since USAG-1 inhibits Wnt and BMP signals, the essential factors for tooth development, via direct binding to BMP and Wnt coreceptor LRP5/6, we hypothesized that USAG-1 plays key regulatory roles in suppressing tooth development. However, the involvement of USAG-1 in various types of congenital tooth agenesis remains unknown. Here, we show that blocking USAG-1 function through USAG-1 knockout or anti–USAG-1 antibody administration relieves congenital tooth agenesis caused by various genetic abnormalities in mice. Our results demonstrate that USAG-1 controls the number of teeth by inhibiting development of potential tooth germs in wild-type or mutant mice missing teeth. Anti–USAG-1 antibody administration is, therefore, a promising approach for tooth regeneration therapy.
Description: 先天性無歯症に対する分子標的薬の開発 --USAG-1を標的分子とした歯再生治療--. 京都大学プレスリリース. 2021-02-15.
Rights: © 2021 The Authors, some rights reserved; exclusive licensee American Association for the Advancement of Science. No claim to original U.S. Government Works. Distributed under a Creative Commons Attribution License 4.0 (CC BY).
This is an open-access article distributed under the terms of the Creative Commons Attribution license, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
URI: http://hdl.handle.net/2433/261703
DOI(Published Version): 10.1126/sciadv.abf1798
PubMed ID: 33579703
Related Link: https://www.kyoto-u.ac.jp/ja/research-news/2021-02-15-0
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