Author

Mangyu Choe

The University of Texas Southwestern Medical CenterORCID 0000-0002-8889-7494Unclaimed ORCID profile · follow to get notified of new preprints

Biology Disciplines

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Biochemistry· 1 Cancer Biology· 1 Systems Biology· 1

Signature Assays, Organisms & Methods

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Research Focus:cell type annotation· 2 Research Focus:gene regulatory network inference· 2 Organism:human· 2 Assay:ATAC-seq· 1 Assay:bulk RNA-seq· 1 Research Focus:cell signaling & trafficking· 1 Research Focus:differential expression· 1 Research Focus:drug response / drug discovery· 1

Frequent Co-Authors

Denis V. TitoviD· 2 shared Alex E. EkvikiD· 1 shared Ariella B. HankeriD· 1 shared Caroline HaueriD· 1 shared Gretchen Stalnaker· 1 shared Hijai R. Shin· 1 shared Hijai R. ShiniD· 1 shared Isaac S. Chan· 1 shared

Activity by Year

2023-2026 · peak 1/yr

Co-Author Collaboration Network

10 top collaborators · 21 mutual co-author links

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2 shared papersSystems Biology

Denis V. TitovORCID

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3 papers

Recent·Most cited

Cancer BiologybioRxivPreprintAug 26, 2026

Tumor control of lysosomal acidification promotes lipoprotein assimilationand ferroptosis resistance

Renfei Wu, Sheng‐Chieh Hsu, Lingjie Sang…·Javier García‐Bermúdez

This study identifies ZNF217 as a driver of tumor lysosomal function and ferroptosis resistance by maintaining lysosomal acidification and lipoprotein assimilation.

DOI 10.64898/2026.08.25.747075

humanproteomics

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Systems BiologyBiophysical JournalPeer-reviewedApr 3, 2025

Data-driven model of glycolysis shows that allostery maintains high ATP levels while mass action controls flux and energy of ATP hydrolysis

Mangyu Choe, Tal Einav, Rob Phillips, Denis V. Titov

14 citationstop 5%

humanmetabolomics

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BiochemistryCell chemical biologyPeer-reviewedDec 27, 2023

Genetically encoded tool for manipulation of Δ{Psi}m identifies the latter as the driver of integrative stress response induced by ATP Synthase dysfunction

Mangyu Choe, Alex E. Ekvik, Gretchen Stalnaker…·Denis V. Titov

The paper develops a genetically encoded tool to manipulate mitochondrial membrane potential and shows it drives the integrated stress response from ATP synthase dysfunction.

4 citations

mouseATAC-seq

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