Author

T. P. Prakash

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

Biology Disciplines

Click to filter author papers

Physiology· 2

Signature Assays, Organisms & Methods

Click to filter · or open tag

Research Focus:cancer & tumor microenvironment· 2 Approach:experimental assay· 2 Organism:mouse· 2 Assay:bulk RNA-seq· 1 Research Focus:cell signaling & trafficking· 1 Research Focus:drug response / drug discovery· 1 Organism:human· 1 Assay:metabolomics· 1

Frequent Co-Authors

A. R. Harrington· 1 shared B. Liu· 1 shared B. Ramms· 1 shared C. Lebeaupin· 1 shared C. Zeng· 1 shared D. P. Pollow· 1 shared E. C. Pirie· 1 shared F. Liu· 1 shared

Activity by Year

2020-2024 · peak 1/yr

Co-Author Collaboration Network

10 top collaborators · 36 mutual co-author links

Click any collaborator node to inspect or filter shared papers

Focal author (center)Selected co-authorORCID co-authorUnlinked name

Curved chords = mutual co-authorship

1 shared paperPhysiology

A. R. Harrington

Mutual co-authors in cluster

Author profile →

2 papers

Recent·Most cited

Metabolic control of adaptive β-cell proliferation by the protein deacetylase SIRT2

M. Wortham, B. Ramms, C. Zeng, J. R. Benthuysen, S. Sai, D. P. Pollow, F. Liu, M. Schlichting, A. R. Harrington, B. Liu, T. P. Prakash, E. C. Pirie, H. Zhu, S. Baghdasarian, J. Auwerx, , M. Sander

This study identifies SIRT2 as a regulator of β-cell proliferation, showing its role in controlling β-cell expansion during hyperglycemia while preserving feedback mechanisms.

bioRxiv · Feb 24, 2024 · PreprintPhysiology

Chop/Ddit3 depletion in β-cells alleviates ER stress and corrects hepatic steatosis

J. Yong, V. P. Parekh, J. Nayak, Z. Chen, C. Lebeaupin, J. Zhang, T. P. Prakash, S. Murray, S. Guo, J. E. Ayala, L. S. Satin, R. J. Kaufman

This study shows that deleting Chop/Ddit3 in β-cells reduces ER stress and corrects fatty liver disease in T2D without affecting glucose homeostasis.

bioRxiv · Jan 2, 2020 · PreprintPhysiology