Author

Farah Diab

InsermORCID 0000-0003-4116-5082Unclaimed ORCID profile · follow to get notified of new preprints

Biology Disciplines

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Developmental Biology· 1 Genetics· 1 Molecular Biology· 1

Signature Assays, Organisms & Methods

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Organism:human· 3 Research Focus:differential expression· 2 Approach:experimental assay· 2 Assay:bulk RNA-seq· 1 Research Focus:cell type annotation· 1 Approach:statistical model· 1

Frequent Co-Authors

Valérie DupéiD· 2 shared Achille AoubaiD· 1 shared Alexandra DesdoitsiD· 1 shared Alexandre NguyeniD· 1 shared Anne CamusiD· 1 shared Aphrodite DaskalopoulouiD· 1 shared Ariane Mahieux· 1 shared Beatriz PuisaciD· 1 shared

Activity by Year

2020-2025 · peak 1/yr

Co-Author Collaboration Network

10 top collaborators · 19 mutual co-author links

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2 shared papersDevelopmental Biology

Valérie DupéORCID

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3 papers

Recent·Most cited

Developmental BiologybioRxivPreprintMay 20, 2025

Mapping the temporal and functional landscape of Sonic Hedgehog signaling reveals new insights into early human forebrain development

Veranika Panasenkava, Jules Garreau, Hélène Guyodo…·Valérie Dupé

This study maps the temporal and functional landscape of Sonic Hedgehog signaling in human forebrain development using stem cell models and identifies new markers of regionalization.

1 citation

humanbulk RNA-seq

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GeneticseLifePeer-reviewedJun 6, 2023

Identification of an A20 critical region harboring missense variations that lead to autoinflammation

Elma El Khouri, Farah Diab, Camille Louvrier…·Irina Giurgea

The paper identifies a critical region in the A20 OTU domain containing missense variations that cause autoinflammation by disrupting NF-κB inhibition.

17 citations

humanstatistical model

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Molecular BiologyCell ReportsPeer-reviewedMay 1, 2020

MAU2 and NIPBL variants in Cornelia de Lange syndrome reveal MAU2-independent loading of cohesin and uncover a protective mechanism against early truncating mutations in NIPBL

Ilaria Parenti, Farah Diab, Sara Ruiz Gil…·Kerstin S. Wendt

The paper investigates variants in MAU2 and NIPBL in CdLS, showing NIPBL haploinsufficiency as the main cause and revealing a protective mechanism for NIPBL out-of-frame mutations.

60 citationstop 3%

humanexperimental assay

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