Thorsten Maretzky

Assistant Professor

Iowa State University

United States

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Thorsten Maretzky is an Assistant Professor at the University of Iowa, USA. His research focuses on areas including T cell differentiation, inflammatory bowel diseases, and the mechanisms of disintegrin and metalloproteases. Recent publications explore the roles of DNA demethylation in CD4 expression and the therapeutic potential of targeting autophagy pathways.

Articles (11)

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2022

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2022

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2022

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2022

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2021

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2021

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2021

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2021

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2021

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2021

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2021

Collaborators (4)

Kristina Thiel

Assistant Professor

Iowa State University

UNITED STATES

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Theresa Lu

Professor

Weill Cornell Medical College

UNITED STATES

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Eric Devor

Research Assistant Professor

The University of Iowa Roy J and Lucille A Carver College of Medicine

UNITED STATES

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Priya Issuree

Iowa State University

UNITED STATES

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Thorsten Maretzky

Research Interests

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Articles (11)

CD4 expression in effector T cells depends on DNA demethylation over a developmentally established stimulus-responsive element.

CD4 expression in effector T cells depends on DNA demethylation over a developmentally established stimulus-responsive element

Targeting the endo-lysosomal autophagy pathway to treat inflammatory bowel diseases.

Targeting the endo-lysosomal autophagy pathway to treat inflammatory bowel diseases

A Disintegrin and Metalloproteases (ADAMs): Activation, Regulation and Mechanisms of Catalysis.

A Disintegrin and Metalloproteases (ADAMs): Activation, Regulation and Mechanisms of Catalysis

Advantages of Tyrosine Kinase Anti-Angiogenic Cediranib over Bevacizumab: Cell Cycle Abrogation and Synergy with Chemotherapy.

Advantages of Tyrosine Kinase Anti-Angiogenic Cediranib over Bevacizumab: Cell Cycle Abrogation and Synergy with Chemotherapy

Targeted truncation of the ADAM17 cytoplasmic domain in mice results in protein destabilization and a hypomorphic phenotype.

Targeted truncation of the ADAM17 cytoplasmic domain in mice results in protein destabilization and a hypomorphic phenotype

Members of the Fibroblast Growth Factor Receptor Superfamily Are Proteolytically Cleaved by Two Differently Activated Metalloproteases.

Collaborators (4)

Kristina Thiel

Theresa Lu

Eric Devor

Priya Issuree

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