Receptor signaling: new insight into its regulatory mechanisms
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- Horinouchi Takahiro
- Department of Cellular Pharmacology, Hokkaido University Graduate School of Medicine, Japan
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- Terada Koji
- Department of Cellular Pharmacology, Hokkaido University Graduate School of Medicine, Japan
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- Higashi Tsunehito
- Department of Cellular Pharmacology, Hokkaido University Graduate School of Medicine, Japan
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- Miwa Soichi
- Department of Cellular Pharmacology, Hokkaido University Graduate School of Medicine, Japan
書誌事項
- タイトル別名
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- Endothelin Receptor Signaling: New Insight Into Its Regulatory Mechanisms
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抄録
The endothelin (ET) system consists of two G protein coupled–receptors (GPCRs), ET type A receptor (ETAR) and ET type B receptor (ETBR), and three endogenous ligands, ET-1, ET-2, and ET-3. Stimulation of ETRs with ET-1 induces an increase in intracellular Ca2+ concentration that is involved in a diverse array of physiological and pathophysiological processes, including vasoconstriction, and cell proliferation. Store-operated Ca2+ entry and receptor-operated Ca2+ entry triggered by activation of ETRs are regulated or modulated by endoplasmic reticulum Ca2+ sensor (stromal interaction molecule 1) and voltage-independent cation channels (transient receptor potential canonical channels and Orai1). The ET-1–induced Ca2+ mobilization results from activation of heterotrimeric G proteins by ETRs. In contrast, GPCR biology including modulation of receptor function and trafficking is regulated by a variety of GPCR interacting proteins (GIPs) that generally interact with the C-terminal domain of GPCRs. The ETR signaling is also regulated by GIPs such as Jun activation domain-binding protein 1. This review focuses on the regulatory mechanisms of the ETR signaling with special attention to the components involved in Ca2+ signaling and to GIPs in the signal transduction, modification, and degradation of ETRs.
収録刊行物
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- Journal of Pharmacological Sciences
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Journal of Pharmacological Sciences 123 (2), 85-101, 2013
公益社団法人 日本薬理学会
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詳細情報 詳細情報について
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- CRID
- 1390001205180672640
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- NII論文ID
- 130003382599
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- NII書誌ID
- AA11806667
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- COI
- 1:CAS:528:DC%2BC3sXhslertr3F
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- ISSN
- 13478648
- 13478613
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- NDL書誌ID
- 024954502
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- PubMed
- 24077109
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- 本文言語コード
- en
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- データソース種別
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- JaLC
- NDL
- Crossref
- PubMed
- CiNii Articles
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- 抄録ライセンスフラグ
- 使用不可