Author

T. Yasumi

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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Research Focus:cell signaling & trafficking· 2 Approach:experimental assay· 2 Research Focus:host-pathogen & immune response· 2 Organism:human· 2 Assay:proteomics· 2 Research Focus:cell type annotation· 1 Research Focus:differential expression· 1

Frequent Co-Authors

M. Nishitani-Isa· 2 shared A. A. d. J. Rasheed· 1 shared A. Iannuzzo· 1 shared A. Insalaco· 1 shared E. Hiejima· 1 shared F. Bhuyan· 1 shared G. Prencipe· 1 shared H. Nihira· 1 shared

Activity by Year

2021-2024 · peak 1/yr

Co-Author Collaboration Network

10 top collaborators · 27 mutual co-author links

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2 shared papersImmunology

M. Nishitani-Isa

Mutual co-authors in cluster

Author profile →

2 papers

Recent·Most cited

Autoinflammatory patients with Golgi-trapped CDC42 exhibit intracellular trafficking defects leading to STING hyperactivation

A. Iannuzzo, S. Delafontaine, R. El Masri, R. Tacine, G. Prencipe, M. Nishitani-Isa, R. T. van Wijck, F. Bhuyan, A. A. d. J. Rasheed, S. Coppola, P. L. van Daele, A. Insalaco, R. Goldbach-Mansky, T. Yasumi, M. Tartaglia, , J. Delon

This study identifies Golgi-trapped CDC42 variants causing STING hyperactivation and IFN elevation in autoinflammatory patients.

bioRxiv · Jan 31, 2024 · PreprintImmunology

Aberrant localization of CDC42 C-terminal variants to the Golgi apparatus drives pyrin inflammasome-dependent autoinflammation

M. Nishitani-Isa, K. Mukai, Y. Honda, H. Nihira, H. Shibata, T. Tanaka, K. Kodama, E. Hiejima, K. Izawa, Y. Kawasaki, M. Osawa, Y. Katata, S. Onodera, T. Watanabe, S. Kure, , T. Yasumi

This study identifies that CDC42 C-terminal variants cause aberrant Golgi localization, leading to pyrin inflammasome activation and autoinflammation.

bioRxiv · Sep 3, 2021Immunology