Author

R. D. Sharma

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· 1 Cell Biology· 1 Immunology· 1 Microbiology· 1

Signature Assays, Organisms & Methods

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Approach:experimental assay· 4 Research Focus:host-pathogen & immune response· 3 Organism:human· 3 Assay:proteomics· 3 Research Focus:cell signaling & trafficking· 2 Research Focus:development & morphogenesis· 2 Organism:mouse· 2 Research Focus:cancer & tumor microenvironment· 1

Frequent Co-Authors

D. Kumar· 3 shared P. Sharma· 3 shared A. Singhal· 2 shared B. Sarkar· 2 shared M. Das· 2 shared S. Howland· 2 shared V. Nandicoori· 2 shared A. Chandramouli· 1 shared

Activity by Year

2019-2024 · peak 2/yr

Co-Author Collaboration Network

10 top collaborators · 35 mutual co-author links

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3 shared papersMicrobiology

D. Kumar

Mutual co-authors in cluster

Author profile →

4 papers

Recent·Most cited

PPARγ mediated enhanced lipid biogenesis fuels Mycobacterium tuberculosis growth in a drug-tolerant hepatocyte environment.

B. Sarkar, J. Singh, M. Yadav, P. Sharma, R. D. Sharma, S. Singh, A. Chandramouli, K. Mehdiratta, A. Kumar, S. S. Kamat, D. S. Ghorpade, D. Mohanty, D. Kumar, R. S. Gokhale

This study shows Mtb induces PPARγ in hepatocytes to create lipid droplets and drug-tolerant environments, contributing to systemic pathogenicity and metabolic impairments during TB infection.

bioRxiv · Feb 2, 2024Microbiology

A mitochondrial quality control mechanism reverses the phagosome maturation arrest caused by Mycobacterium tuberculosis

S. Verma, S. Thakur, M. Das, R. D. Sharma, V. Yadav, P. Sharma, M. Marzuki, S. Foo, G. M. Piperno, M. Z. Khan, B. Mathew, M. Bajpai, J. S. Maras, S. Howland, S. Sarkar, , D. Kumar

This study identifies a mitochondrial quality control mechanism that reverses phagosome maturation arrest caused by Mycobacterium tuberculosis through RAB7 recruitment and lysosomal targeting.

bioRxiv · Dec 1, 2023 · PreprintCell Biology

Ly6G+Granulocytes-derived IL-17 limits protective host responses and promotes tuberculosis pathogenesis

P. Sharma, R. D. Sharma, B. Sarkar, V. Panwar, M. Das, L. Singh, N. Jain, S. Chaturvedi, L. Mehra, A. Rathee, S. Sharma, F. Shihui, A. Lee, P. N. Kumar, P. Das, , D. Kumar

This study identifies IL-17 and COX2 as negative regulators of protective immunity in tuberculosis, showing that Ly6G+ granulocytes are a major source of IL-17 and their inhibition reduces bacterial burden and pathology.

bioRxiv · Oct 5, 2023Immunology

Activation of GPR56, a novel adhesion GPCR, is necessary for nuclear androgen receptor signaling in prostate cells

G. Bagchi, J. P. Singh, M. Dagar, G. Dagar, S. Rawal, R. D. Sharma, R. K. Tyagi

This study shows that GPR56 activation by androgens enhances AR signaling through Rho and cAMP/PKA pathways, and its expression is higher in prostate tumors, suggesting it as a therapeutic target.

bioRxiv · Nov 21, 2019Cancer Biology