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  1. 30 医学部・医学研究科・保健学研究科
  2. 30b 弘前医学 = Hirosaki Medical Journal
  3. 69巻1-4号

Involvement of β-arrestin in Endothelin Receptor Signaling : a Possible Role in the Pathogenesis of Pulmonary Arterial Hypertension

http://hdl.handle.net/10129/00006592
http://hdl.handle.net/10129/00006592
ac1b95c6-8791-47ed-9670-707fb9e33fa5
名前 / ファイル ライセンス アクション
HirosakiMedJ_69(1-4)_146.pdf HirosakiMedJ_69(1-4)_146.pdf (440.5 kB)
Item type 学術雑誌論文 / Journal Article(1)
公開日 2019-04-10
タイトル
タイトル Involvement of β-arrestin in Endothelin Receptor Signaling : a Possible Role in the Pathogenesis of Pulmonary Arterial Hypertension
言語
言語 eng
キーワード
主題Scheme Other
主題 Endothelin
キーワード
主題Scheme Other
主題 β-arrestin
キーワード
主題Scheme Other
主題 G-protein coupled receptor
キーワード
主題Scheme Other
主題 Pulmonary arterial hypertension
資源タイプ
資源タイプ識別子 http://purl.org/coar/resource_type/c_6501
資源タイプ journal article
著者 Narita, Noritomo

× Narita, Noritomo

Narita, Noritomo

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Hanada, Kenji

× Hanada, Kenji

Hanada, Kenji

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Senoo, Maiko

× Senoo, Maiko

Senoo, Maiko

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Kato, Tomo

× Kato, Tomo

Kato, Tomo

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Kudo, Natsumi

× Kudo, Natsumi

Kudo, Natsumi

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Yokono, Yoshikazu

× Yokono, Yoshikazu

Yokono, Yoshikazu

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Tsushima, Michiko

× Tsushima, Michiko

Tsushima, Michiko

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Toyama, Yuichi

× Toyama, Yuichi

Toyama, Yuichi

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Narita, Masato

× Narita, Masato

Narita, Masato

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Tomita, Hirofumi

× Tomita, Hirofumi

Tomita, Hirofumi

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著者所属
値 Department of Cardiology, Hirosaki University Graduate School of Medicine,
抄録
内容記述タイプ Abstract
内容記述 Background: Endothelin (ET) is a strong vasoconstrictor that plays important roles in the pathogenesis and progression of cardiovascular remodeling. ET receptor( ET-R) antagonists have recently become established as a drug essential for treating pulmonary arterial hypertension( PAH). β-arrestin was originally identified as a regulator of G-protein coupled receptor recycling, but it recently became apparent that β-arrestins act as scaffolds in their own signaling pathway. In this study, we examined the role of β-arrestin in ET-R signaling and explored its possible role in the pathogenesis of PAH.
Methods and Results: The knockdown of β-arrestin1 or β-arrestin2 in human kidney embryonic 293 cells resulted in nhanced extracellular signal-regulated kinase (ERK) 1/2 phosphorylation in response to ET. Confocal microscopy showed that, in the absence of stimulation, transiently transfected green fluorescent protein-tagged epidermal growth factor receptors( EGFRs) were located on the plasma membrane, whereas they were internalized in response to ET, as shown by their redistribution into cellular aggregates. Pretreatment with Ro318425( a protein kinase C inhibitor) or AG1478( an EGFR antagonist) suppressed ERK1/2 phosphorylation in response to ET.
Conclusions: β-arrestins and EGFR transactivation are involved in ET-R signaling. These new insights may contribute to elucidating further layers in the pathogenesis of PAH.
書誌情報 弘前医学

巻 69, 号 1-4, p. 146-154, 発行日 2019-03-15
ISSN
収録物識別子タイプ ISSN
収録物識別子 0439-1721
書誌レコードID
収録物識別子タイプ NCID
収録物識別子 AN00211444
著者版フラグ
出版タイプ VoR
出版タイプResource http://purl.org/coar/version/c_970fb48d4fbd8a85
日本十進分類法
主題Scheme NDC
主題 490
出版者
出版者 弘前大学大学院医学研究科・弘前医学会
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