Johannes Graumann

Professor of Translational Proteomics

Philipps-Universität Marburg

Germany

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Johannes Graumann is a Professor of Translational Proteomics at Philipps-Universität Marburg, Germany. His research primarily focuses on the intersections of metabolic pathways in cancer and metabolic diseases, as evidenced by his recent articles on topics such as adipocyte dysfunction, pancreatic islet pathology in type 2 diabetes, and the role of epigenetics in cancer progression. Additionally, he investigates the mechanisms of tumor cell proliferation and the signaling pathways involved in immune cell function.

Articles (20)

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2025

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2022

Collaborators (11)

Haruya Kawase

Max Planck Institute for Heart and Lung Research

GERMANY

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M. Lienhard Schmitz

Full Professor

University of Giessen

GERMANY

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Aina Lluch Balaña

Institut d'Investigació Biomèdica de Girona Dr Josep Trueta

SPAIN

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Jingchen Shao

Max Planck Institute for Heart and Lung Research

GERMANY

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Prof. Joerg Walter Bartsch

Professor/Lab Head

Philipps-Universität Marburg Fachbereich Medizin

GERMANY

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Jan Halbritter

University Hospital Leipzig

GERMANY

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Ralph Schermuly

Professor

GERMANY

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Christian Preußer

Heading EV Core Facility

Philipps-Universität Marburg

GERMANY

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Elke Pogge von Strandmann

GERMANY

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Jose Luis Labandeira-Garcia

Full Professor

Universidade de Santiago de Compostela

SPAIN

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Vicki Hertzberg

Emory University

UNITED STATES

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Johannes Graumann

Research Interests

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Articles (20)

Synergistic targeting of cancer cells through simultaneous inhibition of key metabolic enzymes

SIAH3 is frequently epigenetically silenced in cancer and regulates mitochondrial metabolism

Defective Olfactomedin-2 connects adipocyte dysfunction to obesity.

Multiomics Analysis Reveals Insights into Potential Drivers of Pancreatic Islet Pathology in Type 2 Diabetes

Epigenetic silencing and CRISPR-mediated reactivation of tight junction protein claudin10b (CLDN10B) in renal cancer.

The tumor suppressor FAT1 controls YAP/TAZ protein degradation and tumor cell proliferation through E3 ligase MIB2

Basal cell adhesion molecule (BCAM) promotes mesothelial-to-mesenchymal transition and tumor angiogenesis through paracrine signaling

Nuclear microRNA 9 mediates G-quadruplex formation and 3D genome organization during TGF-β-induced transcription

Arachidonic acid impairs natural killer cell functions by disrupting signaling pathways driven by activating receptors and reactive oxygen species

NoxO1 regulates EGFR signaling by its interaction with Erbin

Impaired Plakophilin-2 in obesity breaks cell cycle dynamics to breed adipocyte senescence

Basal cell adhesion molecule promotes metastasis‐associated processes in ovarian cancer

Systemic Markers of Lung Function and Forced Expiratory Volume in 1 Second Decline across Diverse Cohorts

Menstrual blood-derived mesenchymal stromal cells: impact of preconditioning on the cargo of extracellular vesicles as potential therapeutics

KLF4-mediated upregulation of the NKG2D ligand MICA in acute myeloid leukemia: a novel therapeutic target identified by enChIP

Endothelial FAT1 inhibits angiogenesis by controlling YAP/TAZ protein degradation via E3 ligase MIB2

Epigenetically silenced apoptosis-associated tyrosine kinase (AATK) facilitates a decreased expression of Cyclin D1 and WEE1, phosphorylates TP53 and reduces cell proliferation in a kinase-dependent manner

Isolation of native EVs from primary biofluids—Free‐flow electrophoresis as a novel approach to purify ascites‐derived EVs

ADAR1 Prevents Autoinflammatory Processes in the Heart Mediated by IRF7

Arachidonic acid, a clinically adverse mediator in the ovarian cancer microenvironment, impairs JAK‐STAT signaling in macrophages by perturbing lipid raft structures

Collaborators (11)

Haruya Kawase

M. Lienhard Schmitz

Aina Lluch Balaña

Jingchen Shao

Prof. Joerg Walter Bartsch

Jan Halbritter

Ralph Schermuly

Christian Preußer

Elke Pogge von Strandmann

Jose Luis Labandeira-Garcia

Vicki Hertzberg

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