Benjamin Prosser

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Associate Professor

University of Pennsylvania

United States

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Benjamin Prosser is an Associate Professor at the University of Pennsylvania, USA. His research focus includes the ultrastructural analysis of mitochondria and their role in heart failure, as well as the genetic underpinnings of neurodevelopmental disorders associated with SYNGAP1 and STXBP1 variants. Through his recent publications, he explores therapeutic development and clinical readiness for these complex conditions, with a specific interest in the impact of microtubules and stress responses on cardiac function.

Recent Grants

Grant: Close

MicroRNA site-blocking oligonucleotides as a novel therapy for neurodevelopmental disorders

Open Date: 2021-07-01

Close Date: 2022-12-31

Grant: Close

Mechanical Stress-Dependent Remodeling of the Cardiac Microtubule Network

Open Date: 2020-03-01

Close Date: 2025-02-28

Grant: Close

Cytoskeletal regulation of cardiomyocyte homeostasis in health and disease

Open Date: 2020-01-01

Close Date:

Grant: Close

Targeting micro-RNAs to treat genetic epilepsies

Open Date: 2019-06-01

Close Date: 2020-05-31

Grant: Close

RNA trafficking and localized translation in cardiac homeostasis and hypertrophy

Open Date: 2019-01-01

Close Date:

Articles (20)

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2021

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2021

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2021

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2021

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2020

Collaborators (10)

Kate Baker

UNITED KINGDOM

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Hanna Lammertse

University of Amsterdam

NETHERLANDS

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Elise A. Corbin

UNITED STATES

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Kenneth Margulies

Professor, Clinician-Educator

University of Pennsylvania

UNITED STATES

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Emily Flam

Université de Lille

FRANCE

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Won Hee Lee

Assistant Professor

UNITED STATES

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Ganna Balagura

University of Amsterdam

NETHERLANDS

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Sandra Pinho

Assistant Professor

University of Chicago

UNITED STATES

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Niels Voigt

University Medical Center Göttingen

GERMANY

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Andrey Poleshko

University of Pennsylvania

UNITED STATES

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Benjamin Prosser

Research Interests

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About

Recent Grants

Articles (20)

Ultrastructure analysis of mitochondria, lipid droplet and sarcoplasmic reticulum apposition in human heart failure.

Familial SYNGAP1 variants define the boundaries of a complex neurodevelopmental disorder with epilepsy.

Clinical signatures of SYNGAP1-related disorders through data integration

Microtubules: highway to … arrhythmia?

Integrated Stress Response Potentiates Ponatinib-Induced Cardiotoxicity

Early life seizures and epileptic spasms in STXBP1-related disorders.

Accelerating therapeutic development and clinical trial readiness for STXBP1 and SYNGAP1 disorders

Chronic Activation of Tubulin Tyrosination Improves Heart Function

4. Generation of humanized mouse models to support therapeutic development for SYNGAP1 and STXBP1 disorders.

Integrated Stress Response Potentiates Ponatinib-Induced Cardiotoxicity.

Assessing the landscape of STXBP1-related disorders in 534 individuals

Desmin intermediate filaments and tubulin detyrosination stabilize growing microtubules in the cardiomyocyte.

Extracellular stiffness induces contractile dysfunction in adult cardiomyocytes via cell-autonomous and microtubule-dependent mechanisms.

Base editing the synapse: Modeling a complex neurological disorder in non-human primates.

Truncated titin proteins in dilated cardiomyopathy.

Need for Speed: The Importance of Physiological Strain Rates in Determining Myocardial Stiffness.

X-ROS Signaling Depends on Length-Dependent Calcium Buffering by Troponin.

Cochlear supporting cells require GAS2 for cytoskeletal architecture and hearing.

Pathogenic LMNA variants disrupt cardiac lamina-chromatin interactions and de-repress alternative fate genes.

A Balance between Intermediate Filaments and Microtubules Maintains Nuclear Architecture in the Cardiomyocyte

Collaborators (10)

Kate Baker

Hanna Lammertse

Elise A. Corbin

Kenneth Margulies

Emily Flam

Won Hee Lee

Ganna Balagura

Sandra Pinho

Niels Voigt

Andrey Poleshko

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