Eamonn Dickson

Associate Professor

University of California, Davis

United States

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Eamonn Dickson is an Associate Professor at the University of California Davis, USA. His research focuses on cardiac physiology, neurodegeneration, and the role of various channels, transporters, and receptors in cellular signaling. Recent publications include studies on calcium signaling in relation to heart function and neurotoxicity, with particular emphasis on the interactions between cholesterol and cellular mechanisms in aging and disease.

Articles (14)

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2025

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2020

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2020

Collaborators (10)

Shigeru Chohnan_

Professor

Ibaraki University

JAPAN

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Alfredo J Miñano-Molina

Associate Professor

Universitat Autònoma de Barcelona Facultat de Medicina

SPAIN

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Mary Horne

Adj. Associate Professor

University of California, Davis

UNITED STATES

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Mercedes UNZETA

Full Professor

University of Barcelona

SPAIN

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Padmini Sirish

Associate Adjunct Professor

University of California, Davis

UNITED STATES

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Phung N Thai

University of California, Los Angeles

UNITED STATES

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Johannes W Hell

Professor

University of California, Davis

UNITED STATES

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Jose Rodriguez-Alvarez

Full Professor

University of Barcelona

SPAIN

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Rose Dixon

Assistant Professor

University of California, Davis

UNITED STATES

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James S. Trimmer

UNITED STATES

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Eamonn Dickson

Research Interests

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Articles (14)

14-3-3 promotes sarcolemmal expression of cardiac Ca V 1.2 and nucleates isoproterenol-triggered channel superclustering

Publisher Correction: BIN1 knockdown rescues systolic dysfunction in aging male mouse hearts

BIN1 knockdown rescues systolic dysfunction in aging male mouse hearts

Channels, Transporters, and Receptors at Membrane Contact Sites

Unraveling the Connection: Cholesterol, Calcium Signaling, and Neurodegeneration

Acute phosphatidylinositol 4,5 bisphosphate depletion destabilizes sarcolemmal expression of cardiac L-type Ca 2+ channel Ca V 1.2

NPC1-dependent alterations in KV2.1–CaV1.2 nanodomains drive neuronal death in models of Niemann-Pick Type C disease

α-Synuclein-dependent increases in PIP5K1γ drive inositol signaling to promote neurotoxicity

Phosphoinositide transport and metabolism at membrane contact sites.

IP 3 R-driven increases in mitochondrial Ca 2+ promote neuronal death in NPC disease

NPC1 regulates the distribution of phosphatidylinositol 4‐kinases at Golgi and lysosomal membranes

β-Adrenergic control of sarcolemmal Ca V 1.2 abundance by small GTPase Rab proteins

Sensing of nutrients by CPT1C controls SAC1 activity to regulate AMPA receptor trafficking

AKAP5 complex facilitates purinergic modulation of vascular L-type Ca<sup>2+</sup> channel Ca<sub>V</sub>1.2.

Collaborators (10)

Shigeru Chohnan_

Alfredo J Miñano-Molina

Mary Horne

Mercedes UNZETA

Padmini Sirish

Phung N Thai

Johannes W Hell

Jose Rodriguez-Alvarez

Rose Dixon

James S. Trimmer

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