Author

E. L. Goldberg

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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Immunology· 3 Biochemistry· 1

Signature Assays, Organisms & Methods

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Approach:experimental assay· 4 Research Focus:host-pathogen & immune response· 3 Research Focus:metabolism & bioenergetics· 3 Organism:mouse· 3 Assay:bulk RNA-seq· 2 Research Focus:cell type annotation· 1 Assay:metabolomics· 1 Research Focus:protein folding & dynamics· 1

Frequent Co-Authors

C. D. Camell· 2 shared T. Dlugos· 2 shared V. D. Dixit· 2 shared Y.-H. Youm· 2 shared A. Bartke· 1 shared A. Burlingame· 1 shared A. Lee· 1 shared A. Letian· 1 shared

Activity by Year

2019-2023 · peak 1/yr

Co-Author Collaboration Network

10 top collaborators · 17 mutual co-author links

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2 shared papersImmunology

C. D. Camell

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Author profile →

4 papers

Recent·Most cited

Non-specific recognition of histone modifications by H3K9bhb antibody

T. Tsusaka, J. A. Oses-Prieto, C. Lee, B. DeFelice, A. Burlingame, E. L. Goldberg

The paper shows that the H3K9bhb antibody also recognizes other modifications, including acetylations, which can affect interpretations of gene regulation data.

bioRxiv · Apr 12, 2023Biochemistry

Innate immune cell-intrinsic ketogenesis is dispensable for organismal metabolism and age-related inflammation

E. L. Goldberg, A. Letian, T. Dlugos, C. Leveau, V. D. L. Dixit

This study shows that ketogenesis in innate immune cells is not essential for metabolism or age-related inflammation, but liver-derived ketone bodies are critical for controlling inflammation and metabolism during aging.

bioRxiv · Oct 14, 2022Immunology

Dysregulation of adipose ILC2 underlies thermogenic failure in aging

E. L. Goldberg, I. Shchukina, Y.-H. Youm, C. D. Camell, T. Dlugos, M. Artyomov, V. D. Dixit

The paper identifies age-related changes in adipose tissue that reprogram ILC2, leading to impaired cold tolerance in aged mice.

bioRxiv · Sep 8, 2020 · PreprintImmunology

Aging induces Nlrp3 inflammasome dependent adipose B cell expansion to impair metabolic homeostasis

C. D. Camell, A. Lee, P. Günther, E. L. Goldberg, O. Spadaro, Y.-H. Youm, A. Bartke, G. B. Hubbard, Y. Ikeno, N. H. Ruddle, J. L. Schultz, V. D. Dixit

This study shows aging increases adipose B cells and FALCs via Nlrp3 inflammasome, impairing metabolism, and B cell depletion improves metabolic function in aged mice.

bioRxiv · Apr 13, 2019Immunology