Artikel ; Online: Inhibition of Voltage-Gated Calcium Channels by RGK Proteins.
Current molecular pharmacology
2015 Band 8, Heft 2, Seite(n) 180–187
Abstract: Due to their essential biological roles, voltage-gated calcium channels (VGCCs) are regulated by a myriad of molecules and mechanisms. Fifteen years ago, RGK proteins were discovered to bind the VGCC β subunit (Cavβ) and potently inhibit high-voltage ... ...
Abstract | Due to their essential biological roles, voltage-gated calcium channels (VGCCs) are regulated by a myriad of molecules and mechanisms. Fifteen years ago, RGK proteins were discovered to bind the VGCC β subunit (Cavβ) and potently inhibit high-voltage activated Ca(2+) channels. RGKs (Rad, Rem, Rem2 and Gem/Kir) are a family of monomeric small GTPases belonging to the superfamily of Ras GTPases. They exert dual inhibitory effects on VGCCs, decreasing surface expression and suppressing surface channels through immobilization of the voltage sensor or reduction of channel open probability. While Cavβ is required for all forms of RGK inhibition, not all inhibition is mediated by the RGK-Cavβ interaction. Some RGK proteins also interact directly with the pore-forming α1 subunit of some types of VGCCs (Cavα1). Importantly, RGK proteins tonically inhibit VGCCs in native cells, regulating cardiac and neural functions. This minireview summarizes the mechanisms, molecular determinants, and physiological impact of RGK inhibition of VGCCs. |
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Mesh-Begriff(e) | Animals ; Calcium Channels/chemistry ; Calcium Channels/metabolism ; Humans ; Ion Channel Gating/physiology ; Models, Biological ; Models, Molecular ; Monomeric GTP-Binding Proteins/chemistry ; Monomeric GTP-Binding Proteins/metabolism ; Protein Binding ; Protein Structure, Tertiary ; Protein Subunits/chemistry ; Protein Subunits/metabolism |
Chemische Substanzen | Calcium Channels ; Protein Subunits ; Monomeric GTP-Binding Proteins (EC 3.6.5.2) |
Sprache | Englisch |
Erscheinungsdatum | 2015-05-10 |
Erscheinungsland | United Arab Emirates |
Dokumenttyp | Journal Article ; Research Support, N.I.H., Extramural ; Review |
ISSN | 1874-4702 |
ISSN (online) | 1874-4702 |
DOI | 10.2174/1874467208666150507105613 |
Datenquelle | MEDical Literature Analysis and Retrieval System OnLINE |
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