Author

Diones Bueno

University Medical Center of the Johannes Gutenberg University MainzORCID 0000-0002-8064-6412Unclaimed ORCID profile · follow to get notified of new preprints

Biology Disciplines

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Neuroscience· 2 Cell Biology· 1

Signature Assays, Organisms & Methods

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Approach:experimental assay· 3 Research Focus:cell type annotation· 2 Organism:human· 2 Assay:proteomics· 2 Research Focus:cell signaling & trafficking· 1 Research Focus:cell-cell communication· 1 Research Focus:chromatin & epigenetic regulation· 1 Research Focus:development & morphogenesis· 1

Frequent Co-Authors

Axel MethneriD· 3 shared Liliana Rojas-CharryiD· 3 shared Christina WolfiD· 2 shared Marion SiliesiD· 2 shared Sandra RitziD· 2 shared Sara BitariD· 2 shared Alireza PouyaiD· 1 shared Andrea HellwigiD· 1 shared

Activity by Year

2021-2025 · peak 1/yr

Co-Author Collaboration Network

10 top collaborators · 39 mutual co-author links

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3 shared papersNeuroscience

Axel MethnerORCID

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3 papers

Recent·Most cited

Interaction of the mitochondrial calcium/proton exchanger TMBIM5 with MICU1

Li Zhang, Benjamin Gottschalk, Felicia Dietsche, Sara Bitar, Diones Bueno, Liliana Rojas-Charry, Anshu Kumari, Vivek Garg, Wolfgang F. Graier, Axel Methner

This study investigates the interaction between TMBIM5 and MICU1 in mitochondria, showing they regulate structure, calcium homeostasis, and apoptosis in Drosophila and human cells.

Communications Biology · Sep 19, 2025Peer-reviewedCell Biology

GDAP1 loss of function inhibits the mitochondrial pyruvate dehydrogenase complex by altering the actin cytoskeleton

Christina Wolf, Alireza Pouya, Sara Bitar, Annika Pfeiffer, Diones Bueno, Liliana Rojas-Charry, Sabine Arndt, David Gomez‐Zepeda, Stefan Tenzer, Federica Dal Bello, Caterina Vianello, Sandra Ritz, Jonas Schwirz, Kristina Dobrindt, Michael Peitz, , Axel Methner

This study identifies how GDAP1 loss of function disrupts actin signaling, leading to mitochondrial tubularity and metabolic changes in CMT4A.

Communications Biology · Jun 3, 2022Peer-reviewedNeuroscience

NECAB2 participates in an endosomal pathway of mitochondrial stress response at striatal synapses

Diones Bueno, Partha Narayan Dey, Teresa Schacht, Christina Wolf, Verena Wüllner, Elena Morpurgo, Liliana Rojas-Charry, Lena Sessinghaus, Petra Leukel, Clemens Sommer, Konstantin Radyushkin, Michael K. E. Schäfer, Luise Florin, Jan Baumgart, Paul Stamm, , Axel Methner

This study identifies NECAB2's role in an endosomal pathway for mitochondrial stress response and repair in striatal synapses, linking its loss to synaptic loss and behavioral deficits.

bioRxiv · Feb 15, 2021 · PreprintNeuroscience