Author

E. Topley

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

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Cell Biology· 1

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Assay:bulk RNA-seq· 1 Research Focus:cell signaling & trafficking· 1 Research Focus:differential expression· 1 Approach:experimental assay· 1 Organism:human· 1 Research Focus:metabolism & bioenergetics· 1 Assay:metabolomics· 1 Approach:statistical model· 1

Frequent Co-Authors

B. Bilanges· 1 shared C.-Y. Chung· 1 shared G. E. Valdebenito· 1 shared G. Szabadkai· 1 shared J. H. Ahn· 1 shared J. Tan· 1 shared K. Singh· 1 shared M. R. Duchen· 1 shared

Activity by Year

2020-2020 · peak 1/yr

Co-Author Collaboration Network

10 top collaborators · 45 mutual co-author links

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1 shared paperCell Biology

B. Bilanges

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1 paper

Recent·Most cited

Constitutive activation of the PI3K-Akt-mTORC1 pathway sustains the m.3243A>G mtDNA mutation

C.-Y. Chung, K. Singh, V. N. Kotiadis, G. E. Valdebenito, J. H. Ahn, E. Topley, J. Tan, W. D. Andrews, B. Bilanges, R. D. S. Pitceathly, G. Szabadkai, M. Yuneva, M. R. Duchen

The paper shows that the m.3243A>G mtDNA mutation activates the PI3K-Akt-mTORC1 pathway, which can be inhibited to reduce mutant mtDNA load and improve cellular function.

bioRxiv · Jun 18, 2020 · PreprintCell Biology