Author

N. Dubey

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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Biochemistry· 3 Immunology· 2 Microbiology· 2

Signature Assays, Organisms & Methods

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Approach:experimental assay· 7 Organism:mouse· 5 Research Focus:host-pathogen & immune response· 3 Research Focus:cell signaling & trafficking· 2 Assay:bulk RNA-seq· 1 Research Focus:cell type annotation· 1 Research Focus:chromatin & epigenetic regulation· 1 Research Focus:development & morphogenesis· 1

Frequent Co-Authors

A. Smirnov· 3 shared C. L. Stallings· 3 shared D. Kreamalmeyer· 3 shared R. L. Kinsella· 3 shared R. Woodson· 3 shared S. K. Naik· 3 shared S. R. McKee· 3 shared B. Pal· 2 shared

Activity by Year

2021-2023 · peak 3/yr

Co-Author Collaboration Network

10 top collaborators · 24 mutual co-author links

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Curved chords = mutual co-authorship

3 shared papersImmunology

A. Smirnov

Mutual co-authors in cluster

Author profile →

7 papers

Recent·Most cited

Type I IFN signaling in the absence of IRGM1 promotes M. tuberculosis replication in immune cells by suppressing T cell responses

S. K. Naik, M. E. McNehlan, Y. Mreyoud, R. L. Kinsella, A. Smirnov, C. S. Chowdhury, S. R. McKee, N. Dubey, R. Woodson, D. Kreamalmeyer, C. L. Stallings

This study shows that IRGM1 deletion increases type I IFN signaling, which suppresses T cell responses and promotes M. tuberculosis replication in immune cells.

bioRxiv · Oct 3, 2023 · PreprintImmunology

Unmasking Crucial Residues in Adipose Triglyceride Lipase (ATGL) for Co-Activation with Comparative Gene Identification-58 (CGI-58)

N. Kulminskaya, C. F. Rodriguez Gamez, P. Hofer, I. K. Cerk, N. Dubey, R. Viertlmayr, T. Sagmeister, T. Pavkov-Keller, R. Zechner, M. Oberer

This study identifies key residues in ATGL critical for co-activation with CGI-58 using mutagenesis and AlphaFold modeling.

bioRxiv · Jun 26, 2023Biochemistry

Autophagy functions in lung macrophages and dendritic cells to regulate allergen-dependent inflammatory responses

N. Dubey, R. Woodson, S. V. Hendrix, A. L. Rosen, R. L. Kinsella, S. R. McKee, M. Starick, N. Rivera-Espinal, S. K. Naik, A. Smirnov, D. Kreamalmeyer, A. L. Kau, C. L. Stallings

This study identifies autophagy's role in lung macrophages and dendritic cells in suppressing TH17 responses and neutrophil accumulation in allergic inflammation, with allergen-dependent effects on TH2 responses and cytokine secretion.

bioRxiv · Mar 16, 2023Immunology

Autophagy protects against high-dose Mycobacterium tuberculosis infection

S. Feng, E. M. Nehls, R. L. Kinsella, S. M. Chavez, S. K. Naik, S. R. McKee, N. Dubey, A. Samuels, A. Swain, X. Cui, S. V. Hendrix, R. Woodson, D. Kreamalmeyer, A. Smirnov, M. N. Artyomov, , C. L. Stallings

This study shows autophagy in myeloid cells protects against high-dose Mycobacterium tuberculosis infection by limiting myeloid-derived suppressor cells and promoting T cell responses, distinct from its role in low-dose infection.

bioRxiv · Nov 4, 2022Microbiology

DIP2 is a unique regulator of diacylglycerol lipid homeostasis in eukaryotes

S. Mondal, P. Kinatukara, S. Singh, S. Shambhavi, G. S. Patil, N. Dubey, S. H. Singh, B. Pal, P. C. Shekar, S. S. Kamat, R. Sankaranarayanan

This study identifies DIP2 as a regulator of specific diacylglycerol (DAG) subsets in yeast, fly, and mouse, showing its role in preventing toxic DAG accumulation and modulating lipid homeostasis.

bioRxiv · Feb 7, 2022Biochemistry

A universal pocket in FAALs ensures redirection of fatty acid pool away from CoA-based activation

G. S. Patil, P. Kinatukara, S. Mondal, S. Shambhavi, K. D. Patel, S. Pramanik, N. Dubey, S. Narasimhan, M. K. Madduri, B. Pal, R. S. Gokhale, R. Sankaranarayanan

The paper identifies a unique binding pocket in FAALs that allows them to selectively use holo-ACP over CoA, enabling CoA-independent fatty acid activation and lipid biosynthesis.

bioRxiv · May 4, 2021Biochemistry

Targeting the artemisinin resistant malaria by repositioning of the anti-Hepatitis C Virus drug Alisporivir

A. Chaurasiya, S. Garg, Z. e. Anam, G. Kumari, N. Joshi, J. Kumari, J. Singhal, N. Singh, S. Kaushik, A. Kaur, n. Dubey, P. Srivastava, M. Marothia, M. Kumar, G. Das, , A. Ranganathan

This study repositions Alisporivir, an anti-Hepatitis C drug, as a potential treatment for artemisinin-resistant malaria by targeting PfCyP-19B, which is overexpressed in resistant parasites.

bioRxiv · Jan 8, 2021 · PreprintMicrobiology