Author

D. Braas

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 Immunology· 1 Physiology· 1

Signature Assays, Organisms & Methods

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Approach:experimental assay· 3 Research Focus:cancer & tumor microenvironment· 2 Research Focus:metabolism & bioenergetics· 2 Assay:metabolomics· 2 Organism:mouse· 2 Assay:bulk RNA-seq· 1 Organism:C. elegans· 1 Research Focus:cell type annotation· 1

Frequent Co-Authors

A. A. Vashisht· 1 shared A. J. Clarke· 1 shared A. K. Simon· 1 shared A. Lai· 1 shared A. S. Divakurani· 1 shared B. F. Cravatt· 1 shared B. Lomenick· 1 shared C. Chen· 1 shared

Activity by Year

2017-2022 · peak 1/yr

Co-Author Collaboration Network

10 top collaborators · 14 mutual co-author links

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1 shared paperPhysiology

A. A. Vashisht

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Author profile →

3 papers

Recent·Most cited

The metabolite alpha-ketobutyrate increases health and life spans by activating AMPK

C. Chen, B. Lomenick, M. Chai, W. Huang, J. Chu, L. Vergnes, R. O. Johnson, A. A. Vashisht, R. M. Chin, M. M. Dix, G. Simon, X. Fu, J. C. Link, H. Hwang, X. Yin, , J. Huang

This paper shows that alpha-ketobutyrate extends lifespan and healthspan in C. elegans and mice by activating AMPK through MACF1/VAB-10.

bioRxiv · Oct 10, 2022 · PreprintPhysiology

Glioblastoma utilizes fatty acids and ketone bodies for growth allowing progression during ketogenic diet therapy

J. Sperry, M. C. Condro, L. Guo, K. K. O. Kim, N. Vanderveer-Harris, D. Braas, W. B. Pope, A. S. Divakurani, A. Lai, H. Christofk, J. E. Le Belle, H. I. Kornblum

This study shows that glioblastoma uses fatty acids and ketone bodies for growth, and that ketogenic diet therapy does not effectively inhibit tumor progression.

bioRxiv · Aug 11, 2020Cancer Biology

B1a B cells require autophagy for metabolic homeostasis and self-renewal

A. J. Clarke, T. Riffelmacher, D. Braas, R. J. Cornall, A. K. Simon

This study shows B1a B cells rely on autophagy for metabolic homeostasis and self-renewal, with Atg7 deletion causing their loss due to metabolic dysregulation and mitochondrial dysfunction.

bioRxiv · Dec 28, 2017Immunology