Author

J. Nuechel

Listed by name: these papers carry no ORCID for this author, so different people with the same name may be mixed together.

Biology Disciplines

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Cell Biology· 3

Signature Assays, Organisms & Methods

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Organism:human· 3 Research Focus:cell signaling & trafficking· 2 Research Focus:chromatin & epigenetic regulation· 2 Approach:experimental assay· 2 Research Focus:cell type annotation· 1 Research Focus:differential expression· 1 Assay:DNA methylation· 1 Research Focus:gene regulatory network inference· 1

Frequent Co-Authors

C. Demetriades· 2 shared P. Gollwitzer· 2 shared S. A. Fernandes· 2 shared A. A. Teleman· 1 shared A. Lamprakis· 1 shared A. Sen· 1 shared C. De Virgilio· 1 shared D. Pla-Martin· 1 shared

Activity by Year

2021-2023 · peak 1/yr

Co-Author Collaboration Network

10 top collaborators · 23 mutual co-author links

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2 shared papersCell Biology

C. Demetriades

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Author profile →

3 papers

Recent·Most cited

Spatially and Functionally Distinct mTORC1 Entities Orchestrate the Cellular Response to Amino Acid Availability

S. A. Fernandes, D.-D. Angelidaki, J. Nuechel, J. Pan, P. Gollwitzer, Y. Elkis, F. Artoni, S. Wilhelm, M. Kovacevic-Sarmiento, C. Demetriades

This study reveals spatially and functionally distinct mTORC1 entities that regulate cellular responses to amino acid availability through lysosomal and non-lysosomal mechanisms.

bioRxiv · Oct 3, 2023 · PreprintCell Biology

Malonyl-CoA is an ancient physiological ATP-competitive mTORC1 inhibitor

R. Nicastro, L. Brohee, J. Alba, J. Nuechel, G. Figlia, S. Kipschull, P. Gollwitzer, J. Romero-Pozuelo, S. A. Fernandes, A. Lamprakis, S. Vanni, A. A. Teleman, C. De Virgilio, C. Demetriades

The paper shows malonyl-CoA inhibits mTORC1 by competing with ATP, linking lipid biosynthesis to cellular growth regulation in yeast and mammals.

bioRxiv · Nov 6, 2022 · PreprintCell Biology

Mitochondrial membrane proteins and VPS35 orchestrate selective removal of mtDNA

D. Pla-Martin, A. Sen, S. Kallabis, J. Nuechel, K. Maliphol, J. Hofmann, M. Krueger, R. J. Wiesner

The paper identifies a mechanism involving Twinkle, ATAD3, SAMM50, and VPS35 that selectively removes mutant mtDNA through autophagy, offering therapeutic potential for mtDNA diseases and aging.

bioRxiv · Aug 6, 2021 · PreprintCell Biology