Author

M. K. Jain

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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Cell Biology· 2 Physiology· 1

Signature Assays, Organisms & Methods

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Research Focus:cell type annotation· 3 Research Focus:differential expression· 3 Organism:mouse· 3 Assay:bulk RNA-seq· 2 Approach:experimental assay· 2 Approach:statistical model· 2 Research Focus:gene regulatory network inference· 1 Research Focus:metabolism & bioenergetics· 1

Frequent Co-Authors

A. D. Prabakaran· 1 shared A. Reddy· 1 shared C. Werbrich· 1 shared C. Xu· 1 shared C.-K. Qu· 1 shared D. Mehta· 1 shared D. Prosdocimo· 1 shared D. Weiss· 1 shared

Activity by Year

2023-2023 · peak 3/yr

Co-Author Collaboration Network

10 top collaborators · 14 mutual co-author links

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1 shared paperPhysiology

A. D. Prabakaran

Mutual co-authors in cluster

Author profile →

3 papers

Recent·Most cited

Glucocorticoid chrono-pharmacology unveils novel targets for the cardiomyocyte-specific GR-KLF15 axis in cardiac glucose metabolism

F. El Abdellaoui-Soussi, H. B. Durumutla, H. Latimer, A. D. Prabakaran, K. McFarland, K. Miz, K. Piczer, C. Werbrich, M. K. Jain, S. M. Haldar, M. Quattrocelli

This study identifies the cardiomyocyte-specific GR-KLF15 axis as a circadian-regulated regulator of glucose metabolism, showing that timed glucocorticoid administration improves cardiac function in diabetic mice.

bioRxiv · Dec 18, 2023 · PreprintPhysiology

Tension sensing by FAK governs nuclear mechanotransduction, endothelial transcriptome and fate

M. Z. Akhter, P. Yazbeck, M. Tauseef, M. Anwar, F. Hossen, S. Datta, V. Vellingiri, J. C. Joshi, N. Srivastava, S. Lenzini, G. Zhou, J. Lee, M. K. Jain, J.-W. Shin, D. Mehta

This study shows that FAK-mediated tension sensing in endothelial cells regulates nuclear mechanotransduction, transcriptome, and cell fate, crucial for maintaining a restrictive endothelial barrier.

bioRxiv · Apr 24, 2023 · PreprintCell Biology

Loss of PTPMT1 limits mitochondrial utilization of carbohydrates and leads to muscle atrophy and heart failure in tissue-specific knockout mice

H. Zheng, Q. Li, S. Li, Z. Li, M. Brotto, D. Weiss, D. Prosdocimo, C. Xu, A. Reddy, M. Puchowicz, X. Zhao, M. N. Weitzmann, M. K. Jain, C.-K. Qu

This study shows that PTPMT1 deletion in skeletal muscle and heart causes metabolic inflexibility, leading to atrophy, heart failure, and death, while liver and adipose tissue deletion has no effect.

bioRxiv · Jan 9, 2023 · PreprintCell Biology