Author

Alberto Iannuzzo

Centre National de la Recherche ScientifiqueORCID 0000-0001-8053-2362Unclaimed ORCID profile · follow to get notified of new preprints

Biology Disciplines

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Signature Assays, Organisms & Methods

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

Frequent Co-Authors

Isabelle MeytsiD· 2 shared Jérôme DeloniD· 2 shared Rachida TacineiD· 2 shared Selket DelafontaineiD· 2 shared Adriana A. de JesusiD· 1 shared Antonella InsalacoiD· 1 shared Farzana BhuyaniD· 1 shared Giusi PrencipeiD· 1 shared

Activity by Year

2024-2024 · peak 2/yr

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10 top collaborators · 40 mutual co-author links

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2 shared papersImmunology

Isabelle MeytsORCID

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2 papers

Recent·Most cited

ImmunologyNature CommunicationsPeer-reviewedNov 16, 2024

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

Alberto Iannuzzo, Selket Delafontaine, Rana El Masri…·Jérôme Delon

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

14 citations

humanproteomics

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ImmunologybioRxivPreprintJun 26, 2024

C-terminal CDC42 variants in autoinflammatory patients specifically trigger actin defects and NF-kB hyperactivation

Alberto Iannuzzo, Philippe Mertz, Selket Delafontaine…·Jérôme Delon

The paper investigates four CDC42 variants in autoinflammatory patients, showing that C-terminal variants cause actin defects and NF-kB hyperactivation, while the N-terminal variant does not.

DOI 10.1101/2024.06.26.600829

humanproteomics

𝕏 PostBluesky