Rad and Rem are non-canonical G-proteins with respect to the regulatory role of guanine nucleotide binding in CaV1.2 channel regulation
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Title
Rad and Rem are non-canonical G-proteins with respect to the regulatory role of guanine nucleotide binding in CaV1.2 channel regulation
Authors
Keywords
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Journal
JOURNAL OF PHYSIOLOGY-LONDON
Volume 593, Issue 23, Pages 5075-5090
Publisher
Wiley
Online
2015-10-02
DOI
10.1113/jp270889
References
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Related references
Note: Only part of the references are listed.- Small G Proteins in the Cardiovascular System: Physiological and Pathological Aspects
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- Rad GTPase Deletion Increases L‐type Calcium Channel Current Leading to Increased Cardiac Contraction
- (2013) Janet R. Manning et al. Journal of the American Heart Association
- Structure of the GDP-bound G domain of the RGK protein Rem2
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- Regulation of voltage-dependent calcium channels by RGK proteins
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- Rem-GTPase regulates cardiac myocyte L-type calcium current
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- Distinct RGK GTPases Differentially Use α1- and Auxiliary β-Binding-Dependent Mechanisms to Inhibit CaV1.2/CaV2.2 Channels
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- Molecular Mechanisms, and Selective Pharmacological Rescue, of Rem-Inhibited Ca V 1.2 Channels in Heart
- (2010) Xianghua Xu et al. CIRCULATION RESEARCH
- Rem, a member of the RGK GTPases, inhibits recombinant CaV1.2 channels using multiple mechanisms that require distinct conformations of the GTPase
- (2010) Tingting Yang et al. JOURNAL OF PHYSIOLOGY-LONDON
- Rad As a Novel Regulator of Excitation–Contraction Coupling and β-Adrenergic Signaling in Heart
- (2009) Gang Wang et al. CIRCULATION RESEARCH
- Primary Culture of Adult Rat Heart Myocytes
- (2009) Xianghua Xu et al. Jove-Journal of Visualized Experiments
- Alanine-Scanning Mutagenesis Defines a Conserved Energetic Hotspot in the CaVα1 AID-CaVβ Interaction Site that Is Critical for Channel Modulation
- (2008) Filip Van Petegem et al. STRUCTURE
- The RGK family of GTP-binding proteins: Regulators of voltage-dependent calcium channels and cytoskeleton remodeling
- (2007) Robert N. Correll et al. CELLULAR SIGNALLING
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