Author

Emmanuel Amzallag

Weizmann Institute of ScienceORCID 0009-0008-9423-7776Unclaimed 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· 3 Organism:human· 3 Research Focus:cell-cell communication· 2 Research Focus:differential expression· 2 Research Focus:gene regulatory network inference· 2 Assay:proteomics· 2 Approach:statistical model· 2 Assay:bulk RNA-seq· 1

Frequent Co-Authors

Eran HornsteiniD· 3 shared Yehuda Matan DaninoiD· 2 shared Adam N. TrautwigiD· 1 shared Aleksandar Rajkovic· 1 shared Alicia F. DubinskiiD· 1 shared Alyssa N. CoyneiD· 1 shared Andréanne Lacombe· 1 shared Andrew StrangeiD· 1 shared

Activity by Year

2025-2026 · peak 2/yr

Co-Author Collaboration Network

10 top collaborators · 27 mutual co-author links

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3 shared papersNeuroscience

Eran HornsteinORCID

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3 papers

Recent·Most cited

Cell BiologybioRxivApr 5, 2026

Ubiquitination regulates granulostasis and DRiP accumulation in SGs under heat stress via the E3 ligase MKRN2

Emmanuel Amzallag, Yehuda Matan Danino, Valentina Secco…·Eran Hornstein

This study identifies MKRN2 as an E3 ligase that regulates stress granule dynamics by preventing DRiP accumulation through ubiquitination under heat stress.

DOI 10.6019/s-biad3204

humanproteomics

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NeurosciencebioRxivPreprintSep 17, 2025

TDP-43 pathology triggers SRRM4-dependent cryptic splicing of G3BP1 in ALS/FTD

Hana Fakim, Asmita Ghosh, Emmanuel Amzallag…·Christine Vande Velde

The paper shows that TDP-43 pathology causes a cryptic exon in G3BP1 to be included in neurons, leading to a protein that disrupts stress granule dynamics in ALS/FTD.

3 citations

humanbulk RNA-seq

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NeurosciencebioRxivPreprintApr 20, 2025

TDP-43 toxic gain of function links ALS, FTD and Alzheimers Disease through splicing dysregulation

Welmoed van Zuiden, Thea Deborah Meimoun, Bar Chen…·Eran Hornstein

This study identifies TDP-43-driven splicing dysregulation as a common mechanism in ALS, FTD, and Alzheimer's disease, linking them through mis-spliced mRNAs like APP.

8 citations

humanmetagenomics

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