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Involvement of skin TRPV3 in temperature detection regulated by TMEM79 in mice

発表形態:
原著論文
主要業績:
主要業績
単著・共著:
共著
発表年月:
2023年07月
DOI:
10.1038/s41467-023-39712-x
会議属性:
指定なし
査読:
有り
リンク情報:

日本語フィールド

著者:
*Lei J, Yoshimoto RU, Matsui T, Amagai M, Kido MA, Tominaga M
題名:
Involvement of skin TRPV3 in temperature detection regulated by TMEM79 in mice
発表情報:
Nat Commun 巻: 14 号: 1 ページ: 4104
キーワード:
概要:
TRPV3, a non-selective cation transient receptor potential (TRP) ion channel, is activated by warm temperatures. It is predominantly expressed in skin keratinocytes, and participates in various somatic processes. Previous studies have reported that thermosensation in mice lacking TRPV3 was impaired. Here, we identified a transmembrane protein, TMEM79, that acts as a negative regulator of TRPV3. Heterologous expression of TMEM79 was capable of suppressing TRPV3-mediated currents in HEK293T cells. In addition, TMEM79 modulated TRPV3 translocalization and promoted its degradation in the lysosomes. TRPV3-mediated currents and Ca2+ influx were potentiated in primary mouse keratinocytes lacking TMEM79. Furthermore, TMEM79-deficient male mice preferred a higher temperature than did wild-type mice due to elevated TRPV3 function. Our study revealed unique interactions between TRPV3 and TMEM79, both in vitro and in vivo. These findings support roles for TMEM79 and TRPV3 in thermosensation.
抄録:

英語フィールド

Author:
*Lei J, Yoshimoto RU, Matsui T, Amagai M, Kido MA, Tominaga M
Title:
Involvement of skin TRPV3 in temperature detection regulated by TMEM79 in mice
Announcement information:
Nat Commun Vol: 14 Issue: 1 Page: 4104
An abstract:
TRPV3, a non-selective cation transient receptor potential (TRP) ion channel, is activated by warm temperatures. It is predominantly expressed in skin keratinocytes, and participates in various somatic processes. Previous studies have reported that thermosensation in mice lacking TRPV3 was impaired. Here, we identified a transmembrane protein, TMEM79, that acts as a negative regulator of TRPV3. Heterologous expression of TMEM79 was capable of suppressing TRPV3-mediated currents in HEK293T cells. In addition, TMEM79 modulated TRPV3 translocalization and promoted its degradation in the lysosomes. TRPV3-mediated currents and Ca2+ influx were potentiated in primary mouse keratinocytes lacking TMEM79. Furthermore, TMEM79-deficient male mice preferred a higher temperature than did wild-type mice due to elevated TRPV3 function. Our study revealed unique interactions between TRPV3 and TMEM79, both in vitro and in vivo. These findings support roles for TMEM79 and TRPV3 in thermosensation.


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