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Identification of Potential Modulators of a Pathogenic G Protein-Gated Inwardly Rectifying K⁺ Channel 4 Mutant: In Silico Investigation in the Context of Drug Discovery for Hypertension.

ABSTRACT: Genetic abnormalities have been associated with primary aldosteronism, a major cause of secondary hypertension. This includes mutations in the KCNJ5 gene, which encodes G protein-gated inwardly rectifying K⁺ channel 4 (GIRK4). For example, the substitution of glycine with glutamic acid gives rise to the pathogenic GIRK4^G151E mutation, which alters channel selectivity, making it more permeable to Na⁺ and Ca²⁺. While tertiapin and tertiapin-Q are well-known peptide inhibitors of the GIRK4^WT channel, clinically, there is a need for the development of selective modulators of mutated channels, including GIRK4^G151E. Using in silico methods, including homology modeling, protein-peptide docking, ligand-binding site pre

SUBMITTER: Pitsillou E

PROVIDER: S-EPMC10745636 | biostudies-literature | 2023 Dec

REPOSITORIES: biostudies-literature

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Identification of Potential Modulators of a Pathogenic G Protein-Gated Inwardly Rectifying K⁺ Channel 4 Mutant: In Silico Investigation in the Context of Drug Discovery for Hypertension.

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Dataset Information

Identification of Potential Modulators of a Pathogenic G Protein-Gated Inwardly Rectifying K+ Channel 4 Mutant: In Silico Investigation in the Context of Drug Discovery for Hypertension.

OmicsDI is part of the ELIXIR infrastructure

Tweets

Identification of Potential Modulators of a Pathogenic G Protein-Gated Inwardly Rectifying K⁺ Channel 4 Mutant: In Silico Investigation in the Context of Drug Discovery for Hypertension.