Author

Somesh Sai

Max Delbrück CenterORCID 0000-0001-6865-341XUnclaimed ORCID profile · follow to get notified of new preprints

Biology Disciplines

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Physiology· 2 Cell Biology· 1

Signature Assays, Organisms & Methods

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Approach:experimental assay· 3 Organism:mouse· 3 Approach:statistical model· 3 Research Focus:cell type annotation· 2 Research Focus:differential expression· 2 Assay:scRNA-seq· 2 Assay:bulk RNA-seq· 1 Research Focus:cancer & tumor microenvironment· 1

Frequent Co-Authors

Fenfen Liu· 3 shared Han ZhuiD· 3 shared Maike SanderiD· 3 shared Austin R. Harrington· 2 shared Chun ZengiD· 2 shared Ibrahim Omar· 2 shared Matthew WorthamiD· 2 shared Bastian RammsiD· 1 shared

Activity by Year

2025-2026 · peak 2/yr

Co-Author Collaboration Network

10 top collaborators · 38 mutual co-author links

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3 shared papersPhysiology

Fenfen Liu

Mutual co-authors in cluster

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3 papers

Recent·Most cited

Cell BiologybioRxivPreprintJul 9, 2026

Distinct macrophage and T cell programs shape pancreatic inflammation during metabolic stress and aging

Somesh Sai, Ibrahim Omar, Matthias Barone…·Han Zhu

This study identifies distinct immune mechanisms in pancreatic inflammation during metabolic stress and aging using spatial and single-cell analyses.

DOI 10.64898/2026.07.08.737054

mousespatial transcriptomics

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PhysiologybioRxivPreprintMay 18, 2026

Workload-induced changes to cell state contribute to β-cell failure in diabetes

Somesh Sai, Fenfen Liu, Austin R. Harrington…·Matthew Wortham

This study shows workload-induced β-cell overstimulation leads to failure in T2D, identifying a compensating transcriptional state and the role of Lsd1 in restraining state transitions.

DOI 10.64898/2026.05.13.725004

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PhysiologyJournal of Clinical InvestigationPeer-reviewedJul 31, 2025

Metabolic control of adaptive β-cell proliferation by the protein deacetylase SIRT2

Matthew Wortham, Bastian Ramms, Chun Zeng…·Maike Sander

This study identifies SIRT2 as a regulator of β-cell proliferation, showing its role in controlling β-cell expansion during hyperglycemia while preserving feedback mechanisms.

9 citationstop 5%

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