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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.
DOI(Published Version): 10.1126/sciadv.abf1798
PubMed ID: 33579703
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