Author

T. Pathak

Listed by name: these papers carry no ORCID for this author, so different people with the same name may be mixed together.

Biology Disciplines

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Cancer Biology· 3 Cell Biology· 1 Immunology· 1

Signature Assays, Organisms & Methods

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Approach:experimental assay· 5 Research Focus:cell signaling & trafficking· 4 Research Focus:cancer & tumor microenvironment· 3 Organism:human· 3 Research Focus:metabolism & bioenergetics· 3 Assay:bulk RNA-seq· 2 Approach:mechanistic / dynamical model· 2 Organism:mouse· 2

Frequent Co-Authors

M. Trebak· 5 shared M. T. Johnson· 4 shared P. Xin· 4 shared X. Zhang· 4 shared N. Hempel· 3 shared R. E. Yoast· 3 shared S. M. Emrich· 3 shared V. Walter· 3 shared

Activity by Year

2020-2023 · peak 2/yr

Co-Author Collaboration Network

10 top collaborators · 45 mutual co-author links

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5 shared papersCancer Biology

M. Trebak

Mutual co-authors in cluster

Author profile →

5 papers

Recent·Most cited

Loss of STIM2 in colorectal cancer drives growth and metastasis through metabolic reprogramming and PERK-ATF4 endoplasmic reticulum stress pathway

T. Pathak, J. C. Benson, M. T. Johnson, P. Xin, A. E. Abdelnaby, V. Walter, W. A. Kultun, G. S. Yochum, N. Hempel, M. Trebak

This study shows that loss of STIM2 in colorectal cancer promotes tumor growth and metastasis through metabolic reprogramming and activation of the PERK-ATF4 ER stress pathway.

bioRxiv · Oct 2, 2023 · PreprintCancer Biology

Orai3 and Orai1 are essential for CRAC channel function and metabolic reprogramming in B cells

S. M. Emrich, R. E. Yoast, X. Zhang, A. J. Fike, Y.-H. Wang, K. N. Bricker, A. Tao, P. Xin, V. Walter, M. T. Johnson, T. Pathak, A. C. Straub, S. Feske, Z. Rahman, M. Trebak

This study shows Orai1 and Orai3 are essential for CRAC channel function and metabolic reprogramming in B cells, impacting proliferation, survival, and metabolic processes.

bioRxiv · May 6, 2022Immunology

Curcumin and NCLX Inhibitors Share Anti-Tumoral Mechanisms in Microsatellite-Instability-Driven Colorectal Cancer

M. Gueguinou, S. Ibrahim, J. Bourgeais, A. Robert, T. Pathak, X. Zhang, D. Crottes, J. Dupuy, D. Ternant, V. Monbet, R. Guibon, H. Flores-Romero, A. Lefevre, S. Lerondel, A. Le Pape, , T. Lecomte

This study identifies NCLX as a therapeutic target in MSI-driven CRC, showing that curcumin and NCLX inhibitors induce anti-tumoral effects through mitochondrial calcium overload and apoptosis.

bioRxiv · Jan 18, 2022Cancer Biology

Regulation of Interorganellar Ca2+ Transfer and NFAT Activation by the Mitochondrial Ca2+ Uniporter

R. E. Yoast, S. M. Emrich, X. Zhang, P. Xin, V. Arige, T. Pathak, J. C. Benson, M. T. Johnson, N. Lakomski, N. Hempel, J. M. Han, G. Dupont, D. I. Yule, J. Sneyd, M. Trebak

This study investigates how mitochondrial Ca2+ uniporter (MCU) regulates interorganellar Ca2+ signaling and NFAT activation, showing that MCU-KO increases cytosolic Ca2+ despite reduced CRAC channel activity.

bioRxiv · Apr 7, 2021Cell Biology

Colorectal adenocarcinomas downregulate the mitochondrial Na+/Ca2+ exchanger NCLX to drive metastatic spread

T. Pathak, M. Gueguinou, V. Walter, C. Delierneux, M. T. Johnson, X. Zhang, P. Xin, R. E. Yoast, S. M. Emrich, G. S. Yochum, I. Sekler, W. A. Koltun, D. L. Gill, N. Hempel, M. Trebak

This study shows that reduced NCLX expression in colorectal tumors leads to mtCa2+ overload, promoting metastasis and chemoresistance through mtROS/HIF1 signaling.

bioRxiv · May 7, 2020 · PreprintCancer Biology