心筋L型Ca<SUP>2+</SUP> チャネルのCa<SUP>2+</SUP> 依存性促進および不活性化におけるカルモジュリンおよびCa<SUP>2+</SUP>/カルモジュリン依存性キナーゼIIの異なる役割
-
- 聶 宏光
- Department of Physiology, Graduate School of Medical & Dental Sciences, Kagoshima University, Kagoshima, Japan School of Pharmaceutical Sciences, China Medical University, Shenyang, China
-
- はお 麗英
- Department of Physiology, Graduate School of Medical & Dental Sciences, Kagoshima University, Kagoshima, Japan School of Pharmaceutical Sciences, China Medical University, Shenyang, China
-
- 徐 建軍
- Department of Physiology, Graduate School of Medical & Dental Sciences, Kagoshima University, Kagoshima, Japan
-
- 蓑部 悦子
- Department of Physiology, Graduate School of Medical & Dental Sciences, Kagoshima University, Kagoshima, Japan
-
- 亀山 亜砂子
- Department of Physiology, Graduate School of Medical & Dental Sciences, Kagoshima University, Kagoshima, Japan
-
- 亀山 正樹
- Department of Physiology, Graduate School of Medical & Dental Sciences, Kagoshima University, Kagoshima, Japan
書誌事項
- タイトル別名
-
- Distinct roles of CaM and Ca<SUP>2+</SUP>/CaM-dependent protein kinase II in Ca<SUP>2+</SUP>-dependent facilitation and inactivation of cardiac L-type Ca<SUP>2+</SUP> channels
抄録
L-type Ca2+ channels have two opposing forms of autoregulatory feedback, Ca2+-dependent facilitation (CDF) and Ca2+-dependent inactivation (CDI). To explore the underlying mechanisms, we investigated the effects of CaM and CaMKII inhibitors on CDF and CDI with patch clamp technique in guinea-pig ventricular myocytes. We found that both CDF and CDI were depressed and finally abolished by CaM inhibitors, chlorpromazine (1-100 μM) and calmidazolium (1 μM). In contrast, CaMKII inhibitors, KN-62 (0.1-3 μM) and autocamtide 2-related inhibitory peptide (1 μM), delayed the development of CDF and CDI significantly, but did not depress both CDF and CDI. A CaM-binding GST-fusion peptide containing a. a. 1509-1791 of the C-terminal region of guinea-pig Cav1.2 (CT1) is prepared. In pull-down assay, CT1 treated with CaMKII shows a higher affinity for CaM than that treated with phosphatase. Conclusion: Both CaMKII phosphorylation and binding of CaM to the channel are involved in the process of CDF and CDI. We propose a hypothesis that CaM is a key molecule to bifurcate Ca2+ signal to CDF and CDI, while CaMKII plays a modulatory role. Acknowledgements: This work was supported by the grants from the Japan Society for the Promotion of Science and the National Natural Science Foundation of China (No.30670761). [J Physiol Sci. 2008;58 Suppl:S46]
収録刊行物
-
- 日本生理学会大会発表要旨集
-
日本生理学会大会発表要旨集 2008 (0), 046-046, 2008
一般社団法人 日本生理学会
- Tweet
キーワード
詳細情報 詳細情報について
-
- CRID
- 1390282680706570752
-
- NII論文ID
- 130007039495
-
- データソース種別
-
- JaLC
- CiNii Articles
-
- 抄録ライセンスフラグ
- 使用不可