Author

D. S. Libich

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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Biophysics· 2 Cancer Biology· 1

Signature Assays, Organisms & Methods

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Approach:experimental assay· 3 Approach:biophysical modeling· 1 Research Focus:cancer & tumor microenvironment· 1 Research Focus:cell signaling & trafficking· 1 Research Focus:cell type annotation· 1 Research Focus:differential expression· 1 Research Focus:gene regulatory network inference· 1 Research Focus:protein folding & dynamics· 1

Frequent Co-Authors

A. Baudin· 2 shared X. Xu· 2 shared A. Bandyopadhyay· 1 shared A. E. Lipsitt· 1 shared A. K. Challa· 1 shared A. K. Moreno-Romero· 1 shared A. K. Romero-Moreno· 1 shared A. R. Gilbert· 1 shared

Activity by Year

2021-2023 · peak 1/yr

Co-Author Collaboration Network

10 top collaborators · 22 mutual co-author links

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2 shared papersBiophysics

A. Baudin

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Author profile →

3 papers

Recent·Most cited

Insights into Molecular Diversity within the FET Family: Unraveling Phase Separation of the N-Terminal Low Complexity Domain from RNA-Binding Protein EWS

C. N. Johnson, K. A. Sojitra, E. J. Sohn, A. K. Moreno-Romero, A. Baudin, X. Xu, J. Mittal, D. S. Libich

This study investigates the phase separation mechanism of the EWSLCD domain using biophysical methods, revealing tyrosine residues as key drivers of condensate formation.

bioRxiv · Oct 27, 2023 · PreprintBiophysics

The oncogenic fusion protein EWS-FLI1 promotes premature ageing of biomolecular condensates by catalyzing fibril formation.

E. E. Selig, A. K. Romero-Moreno, S. Akula, X. Xu, D. S. Libich

This study shows EWS-FLI1 promotes premature ageing of biomolecular condensates by catalyzing fibril formation through interactions with EWSLCD.

bioRxiv · Jun 4, 2022 · PreprintBiophysics

Defining function of wild-type and patient specific TP53 mutations in a zebrafish model of embryonal rhabdomyosarcoma

J. Chen, K. Baxi, A. E. Lipsitt, N. R. Hensch, L. Wang, A. Baudin, D. G. Robledo, A. Bandyopadhyay, A. Sugalski, A. K. Challa, A. R. Gilbert, G. E. Tomlinson, P. Houghton, E. Y. Chen, D. S. Libich, M. S. Ignatius

The paper defines the role of wild-type and patient-specific TP53 mutations in ERMS using zebrafish models, showing tp53 loss increases tumor initiation and identifying mutation-specific effects on tumor development.

bioRxiv · Apr 21, 2021Cancer Biology