Coeli M B相关文献与解析，生知库 | 链接生命科学的每一步

The auxiliary subunit KCNE1 regulates KCNQ1 channel response to sustained calcium-dependent PKC activation

辅助亚基 KCNE1 调节 KCNQ1 通道对持续钙依赖性 PKC 激活的响应

期刊:PLoS One

影响因子:2.9

doi:10.1371/journal.pone.0237591

Xiaorong Xu Parks, Haani Qudsi, Chen Braun, Coeli M B Lopes

PKC

发表日期：2020

文献求助收藏

Adrenergic signaling controls RGK-dependent trafficking of cardiac voltage-gated L-type Ca2+ channels through PKD1

肾上腺素能信号通过PKD1控制RGK依赖的心脏电压门控L型Ca2+通道的转运。

期刊:Circulation Research

影响因子:16.2

doi:10.1161/CIRCRESAHA.111.254672

Jhun, Bong Sook; O-Uchi, Jin; Wang, Weiye; Ha, Chang Hoon; Zhao, Jinjing; Kim, Ji Young; Wong, Chelsea; Dirksen, Robert T; Lopes, Coeli M B; Jin, Zheng Gen

Ion channel mechanisms related to sudden cardiac death in phenotype-negative long-QT syndrome genotype-phenotype correlations of the KCNQ1(S349W) mutation.

与表型阴性长QT综合征中猝死相关的离子通道机制 KCNQ1(S349W)突变的基因型-表型相关性

期刊:Journal of Cardiovascular Electrophysiology

影响因子:2.6

doi:10.1111/j.1540-8167.2010.01852.x

Horr Samuel, Goldenberg Ilan, Moss Arthur J, O-Uchi Jin, Barsheshet Alon, Connelly Heather, Gray Daniel A, Zareba Wojciech, Lopes Coeli M B

发表日期：2011

文献求助收藏

A novel mitochondrial K(ATP) channel assay

一种新型线粒体K(ATP)通道检测方法

期刊:Circulation Research

影响因子:16.2

doi:10.1161/CIRCRESAHA.109.215400

Wojtovich, Andrew P; Williams, David M; Karcz, Marcin K; Lopes, Coeli M B; Gray, Daniel A; Nehrke, Keith W; Brookes, Paul S

线粒体

发表日期：2010

文献求助收藏

Small molecule disruption of G beta gamma signaling inhibits the progression of heart failure

小分子干扰Gβγ信号通路可抑制心力衰竭的进展。

期刊:Circulation Research

影响因子:16.2

doi:10.1161/CIRCRESAHA.110.217075

Casey, Liam M; Pistner, Andrew R; Belmonte, Stephen L; Migdalovich, Dmitriy; Stolpnik, Olga; Nwakanma, Frances E; Vorobiof, Gabriel; Dunaevsky, Olga; Matavel, Alessandra; Lopes, Coeli M B; Smrcka, Alan V; Blaxall, Burns C

Molecular basis of decreased Kir4.1 function in SeSAME/EAST syndrome

SeSAME/EAST 综合征中 Kir4.1 功能下降的分子基础

期刊:Journal of the American Society of Nephrology

影响因子:10.3

doi:10.1681/ASN.2009121227

David M Williams, Coeli M B Lopes, Avia Rosenhouse-Dantsker, Heather L Connelly, Alessandra Matavel, Jin O-Uchi, Elena McBeath, Daniel A Gray

信号转导

发表日期：2010

文献求助收藏

PKC activation and PIP(2) depletion underlie biphasic regulation of IKs by Gq-coupled receptors

PKC激活和PIP(2)耗竭是Gq偶联受体对IKs进行双相调节的基础

期刊:Journal of Molecular and Cellular Cardiology

影响因子:4.7

doi:10.1016/j.yjmcc.2009.02.006

Matavel, Alessandra; Lopes, Coeli M B

PIP2 hydrolysis underlies agonist-induced inhibition and regulates voltage gating of two-pore domain K+ channels

PIP2 水解是激动剂诱导抑制的基础，并调节双孔域 K+ 通道的电压门控

期刊:Journal of Physiology-London

影响因子:2.1

doi:10.1113/jphysiol.2004.081935

Coeli M B Lopes, Tibor Rohács, Gábor Czirják, Tamás Balla, Péter Enyedi, Diomedes E Logothetis

发表日期：2005

文献求助收藏

Specificity of activation by phosphoinositides determines lipid regulation of Kir channels

磷脂酰肌醇激活的特异性决定了脂质对Kir通道的调控

期刊:Proceedings of the National Academy of Sciences of the United States of America

影响因子:9.1

doi:10.1073/pnas.0236364100

Rohács, Tibor; Lopes, Coeli M B; Jin, Taihao; Ramdya, Pavan P; Molnár, Zoltán; Logothetis, Diomedes E

信号转导

发表日期：2003

文献求助收藏

Membrane pools of phosphatidylinositol-4-phosphate regulate KCNQ1/KCNE1 membrane expression

磷脂酰肌醇-4-磷酸的膜池调节KCNQ1/KCNE1膜表达

The auxiliary subunit KCNE1 regulates KCNQ1 channel response to sustained calcium-dependent PKC activation

辅助亚基 KCNE1 调节 KCNQ1 通道对持续钙依赖性 PKC 激活的响应

Adrenergic signaling controls RGK-dependent trafficking of cardiac voltage-gated L-type Ca2+ channels through PKD1

肾上腺素能信号通过PKD1控制RGK依赖的心脏电压门控L型Ca2+通道的转运。

Ion channel mechanisms related to sudden cardiac death in phenotype-negative long-QT syndrome genotype-phenotype correlations of the KCNQ1(S349W) mutation.

与表型阴性长QT综合征中猝死相关的离子通道机制 KCNQ1(S349W)突变的基因型-表型相关性

A novel mitochondrial K(ATP) channel assay

一种新型线粒体K(ATP)通道检测方法

Small molecule disruption of G beta gamma signaling inhibits the progression of heart failure

小分子干扰Gβγ信号通路可抑制心力衰竭的进展。

Molecular basis of decreased Kir4.1 function in SeSAME/EAST syndrome

SeSAME/EAST 综合征中 Kir4.1 功能下降的分子基础

PKC activation and PIP(2) depletion underlie biphasic regulation of IKs by Gq-coupled receptors

PKC激活和PIP(2)耗竭是Gq偶联受体对IKs进行双相调节的基础

PIP2 hydrolysis underlies agonist-induced inhibition and regulates voltage gating of two-pore domain K+ channels

PIP2 水解是激动剂诱导抑制的基础，并调节双孔域 K+ 通道的电压门控

Specificity of activation by phosphoinositides determines lipid regulation of Kir channels

磷脂酰肌醇激活的特异性决定了脂质对Kir通道的调控