Author

G. Szabadkai

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

Biology Disciplines

Click to filter author papers

Cell Biology· 3 Cancer Biology· 1

Signature Assays, Organisms & Methods

Click to filter · or open tag

Research Focus:cell signaling & trafficking· 3 Approach:experimental assay· 3 Organism:human· 3 Assay:metabolomics· 3 Research Focus:cancer & tumor microenvironment· 2 Approach:statistical model· 2 Assay:bulk RNA-seq· 1 Research Focus:development & morphogenesis· 1

Frequent Co-Authors

C. Frezza· 2 shared A. Hamacher-Brady· 1 shared A. Nagano· 1 shared A. S. Costa· 1 shared A. Singh· 1 shared B. Bilanges· 1 shared B. Yaman· 1 shared C. Chelala· 1 shared

Activity by Year

2019-2020 · peak 2/yr

Co-Author Collaboration Network

10 top collaborators · 11 mutual co-author links

Click any collaborator node to inspect or filter shared papers

Focal author (center)Selected co-authorORCID co-authorUnlinked name

Curved chords = mutual co-authorship

2 shared papersCancer Biology

C. Frezza

Mutual co-authors in cluster

Author profile →

4 papers

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

Mitochondria form contact sites with the nucleus to couple pro-survival retrograde response

R. Desai, D. A. East, L. Hardy, M. Rigon, D. Faccenda, M. S. Alvarex, A. Singh, M. Mainenti, L. K. Hussey, R. Bentham, G. Szabadkai, V. Zappulli, G. Dhoot, L. E. Romano, X. Dong, , M. Campanella

The paper shows mitochondria form contact sites with the nucleus to facilitate a pro-survival retrograde response by stabilizing transcription factors like NF-kB.

bioRxiv · May 7, 2020 · PreprintCell Biology

The breast cancer oncogene IKKε coordinates mitochondrial function and serine metabolism

R. Xu, W. Jones, E. Wilcz-Villega, S. Costa, V. Rajeeve, R. B. Bentham, K. Bryson, A. Nagano, B. Yaman, S. Olendo Barasa, Y. Wang, C. Chelala, P. Cutillas, G. Szabadkai, C. Frezza, K. Bianchi

This study shows that IKKε, a breast cancer oncogene, reprograms mitochondrial function and serine metabolism independently of its canonical signaling role, promoting cancer cell proliferation.

bioRxiv · Nov 26, 2019Cancer Biology

CHCHD4 regulates a proliferation-EMT switch in tumour cells, through respiratory complex I mediated metabolism.

L. W. Thomas, C. Esposito, J. M. Stephen, A. S. Costa, C. Frezza, T. S. Blacker, G. Szabadkai, M. Ashcroft

This study shows CHCHD4 promotes tumour cell proliferation and suppresses EMT through complex I-mediated mitochondrial metabolism.

bioRxiv · Jan 7, 2019 · PreprintCell Biology