Author

J. C. Crow

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· 4 Microbiology· 1

Signature Assays, Organisms & Methods

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Approach:experimental assay· 4 Organism:human· 4 Assay:bulk RNA-seq· 3 Assay:ChIP-seq· 2 Research Focus:chromatin & epigenetic regulation· 2 Research Focus:drug response / drug discovery· 2 Research Focus:cell type annotation· 1 Organism:E. coli· 1

Frequent Co-Authors

C. Taslim· 4 shared E. R. Theisen· 4 shared S. L. Lessnick· 4 shared I. A. Showpnil· 3 shared J. Selich-Anderson· 3 shared M. A. Boone· 2 shared A. Bayanjargal· 1 shared A. Kasumova· 1 shared

Activity by Year

2020-2024 · peak 2/yr

Co-Author Collaboration Network

10 top collaborators · 33 mutual co-author links

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4 shared papersCancer Biology

C. Taslim

Mutual co-authors in cluster

Author profile →

5 papers

Recent·Most cited

DBD-α4 helix of EWSR1::FLI1 is required for GGAA microsatellite binding that underlies genome regulation in Ewing sarcoma

A. Bayanjargal, C. Taslim, I. A. Showpnil, J. Selich-Anderson, J. C. Crow, R. Zhou, S. L. Lessnick, E. R. Theisen

This study investigates the role of the DBD-4 helix in EWSR1::FLI1's binding to GGAA microsatellites, showing its importance in genome regulation and oncogenic transformation in Ewing sarcoma.

bioRxiv · Jan 31, 2024Cancer Biology

Dynamics of drug delivery determines course of evolution of antibiotic responses in bacteria

J. C. Crow, H. Geng, T. J. Sullivan, S. M. Soucy, D. Schultz

This study shows that the dynamics of antibiotic exposure influence the type of mutations that evolve in bacteria, with gradual exposure leading to adaptive mutations and periodic exposure causing loss of regulatory control.

bioRxiv · Nov 29, 2023 · PreprintMicrobiology

Mitochondrial Dysfunction is a Driver for SP-2509 Drug Resistance in Ewing Sarcoma

E. J. P. Tokarsky, J. C. Crow, L. M. Guenther, J. Sherman, C. Taslim, G. Alexe, K. I. Pishas, G. Rask, B. S. Justis, A. Kasumova, K. Stegmaier, S. L. Lessnick, E. R. Theisen

The paper identifies mitochondrial dysfunction as a mechanism of resistance to the LSD1 inhibitor SP-2509 in Ewing sarcoma and suggests combining LSD1 inhibitors with mitochondrial-targeting agents.

bioRxiv · Dec 13, 2021Cancer Biology

EWS/FLI mediated reprogramming of 3D chromatin promotes an altered transcriptional state in Ewing sarcoma

I. A. Showpnil, J. Selich-Anderson, C. Taslim, M. A. Boone, J. C. Crow, E. R. Theisen, S. L. Lessnick

This study identifies how EWS/FLI fusion proteins alter chromatin structure and transcription in Ewing sarcoma, highlighting their role in reprogramming 3D chromatin to drive transcriptional changes.

bioRxiv · Sep 30, 2021Cancer Biology

The FLI portion of EWS/FLI contributes a transcriptional regulatory function that is distinct and separable from its DNA-binding function in Ewing sarcoma

M. A. Boone, C. Taslim, J. C. Crow, J. Selich-Anderson, I. A. Showpnil, B. D. Sunkel, M. Wang, B. Z. Stanton, E. R. Theisen, S. L. Lessnick

This study identifies the specific FLI regions in EWS/FLI critical for oncogenic transformation in Ewing sarcoma, showing the DNA-binding domain and a carboxyl-terminal alpha-helix are essential for transcriptional regulation and tumorigenesis.

bioRxiv · Oct 29, 2020Cancer Biology