Author

J. Chae

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· 2 Cancer Biology· 1 Cell Biology· 1

Signature Assays, Organisms & Methods

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Approach:experimental assay· 3 Research Focus:drug response / drug discovery· 2 Organism:human· 2 Assay:bulk RNA-seq· 1 Research Focus:cell signaling & trafficking· 1 Research Focus:cell type annotation· 1 Assay:proteomics· 1 Approach:statistical model· 1

Frequent Co-Authors

A. H. Limper· 1 shared B. S. Hong· 1 shared C. Braun· 1 shared C. H. Kim· 1 shared C.-M. Ghim· 1 shared D.-S. Lee· 1 shared D.-Y. Noh· 1 shared H.-B. Lee· 1 shared

Activity by Year

2020-2023 · peak 2/yr

Co-Author Collaboration Network

10 top collaborators · 12 mutual co-author links

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1 shared paperCell Biology

A. H. Limper

Mutual co-authors in cluster

Author profile →

4 papers

Recent·Most cited

Serum albumin maintains Wnt water-solubility and activity

J. H. Yeo, S. S. Kwon, J. Chae, I. Kusen, J. Han, J. Y. Lim, J.-H. Cheong, T. I. Kim, Y. O. Jung, C. H. Kim, J. Lee

This study identifies serum albumin as a factor that maintains Wnt3a solubility and activity, enabling the development of serum-free Wnt3a preparations for therapeutic use.

bioRxiv · Jan 22, 2023 · PreprintBiochemistry

Generalized Michaelis-Menten rate law with time-varying molecular concentrations

R. Lim, T. L. P. Martin, J. Chae, W. Kim, C.-M. Ghim, P.-J. Kim

This paper generalizes the Michaelis-Menten rate law to account for time-varying molecular concentrations by introducing the effective time-delay scheme (ETS).

bioRxiv · Jan 7, 2022Biochemistry

Inhibition of fibrosis with multi-agent therapy in pulmonary fibrosis: Results of a drug library screening

C. Braun, M. Girtman, P. Jenson, M. H. Bourne, J. Chae, T. J. Kottom, A. H. Limper

This study screens FDA-approved drugs to identify synergistic combinations for treating pulmonary fibrosis, finding that azole antifungals may enhance anti-fibrotic effects when combined with existing therapies.

bioRxiv · Jun 29, 2020 · PreprintCell Biology

S100A8/A9 mediate the reprograming of normal mammary epithelial cells induced by dynamic cell-cell interactions with adjacent breast cancer cells.

S. H. Jo, W. H. Heo, M. Quan, B. S. Hong, J. H. Kim, H.-B. Lee, W. Han, Y. Park, D.-S. Lee, N. H. Kwon, M. C. Park, J. Chae, J.-I. Kim, D.-Y. Noh, H.-G. Moon

This study shows that S100A8/A9 mediates the reprogramming of normal mammary epithelial cells by dynamic interactions with breast cancer cells, leading to epithelial-mesenchymal transition and altered cellular behaviors.

bioRxiv · May 2, 2020Cancer Biology