Author

Delphine Stephan

Centre National de la Recherche ScientifiqueORCID 0000-0002-0615-9317Unclaimed ORCID profile · follow to get notified of new preprints

Biology Disciplines

Click to filter author papers

Neuroscience· 2 Cell Biology· 1

Signature Assays, Organisms & Methods

Click to filter · or open tag

Approach:experimental assay· 3 Organism:human· 3 Research Focus:drug response / drug discovery· 2 Research Focus:benchmarking· 1 Assay:bulk RNA-seq· 1 Research Focus:differential expression· 1 Research Focus:gene regulatory network inference· 1 Assay:proteomics· 1

Frequent Co-Authors

Emmanuel NivetiD· 3 shared Santiago RiveraiD· 3 shared Kévin BarangeriD· 2 shared Laura García‐GonzáleziD· 2 shared Laurence LouisiD· 2 shared Michel KhrestchatiskyiD· 2 shared Nicolas JullieniD· 2 shared Angélique Jimenez· 1 shared

Activity by Year

2021-2025 · peak 2/yr

Co-Author Collaboration Network

10 top collaborators · 37 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

3 shared papersNeuroscience

Emmanuel NivetORCID

Mutual co-authors in cluster

Author profile →

3 papers

Recent·Most cited

Cell BiologybioRxivPreprintMay 22, 2025

MT5-MMP C-terminal mutations reduce C99 and β accumulation: A foundation for peptide-based Alzheimer's interventions

Pedro Belio Mairal, Athina Kamitsou, Delphine Stephan…·Santiago Rivera

This study shows that specific mutations in the C-terminal domains of MT5-MMP reduce C99 and Aβ levels, suggesting a potential therapeutic strategy for Alzheimer's disease.

1 citation

humanproteomics

𝕏 PostBluesky

NeuroscienceThe FASEB JournalPeer-reviewedJun 12, 2021

MT5-MMP controls APP metabolism and the fate of beta-CTF/C99 and Abeta through proteolytic-dependent and -independent mechanisms relevant for Alzheimer's disease

Laura García‐González, Jean‐Michel Paumier, Laurence Louis…·Santiago Rivera

This study identifies MT5-MMP's role in regulating APP processing and Aβ levels through proteolytic and non-proteolytic mechanisms in Alzheimer's disease.

17 citations

humanexperimental assay

𝕏 PostBluesky

NeurosciencebioRxivPreprintApr 16, 2021

The Alzheimer's disease risk factor APOE4 drives pro-inflammation in human astrocytes via HDAC-dependent repression of TAGLN3

Laurie Arnaud, Philippe D. Benech, Louise Greetham…·Emmanuel Nivet

This study shows APOE4 promotes inflammation in human astrocytes by repressing TAGLN3 through HDAC activity, linking it to Alzheimer's disease pathology.

5 citations

humanbulk RNA-seq

𝕏 PostBluesky