Author

Emily M. Welebob

Thomas Jefferson University

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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Neuroscience· 2 Biochemistry· 1

Signature Assays, Organisms & Methods

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Assay:bulk RNA-seq· 2 Research Focus:cell type annotation· 2 Research Focus:differential expression· 2 Organism:human· 2 Approach:statistical model· 2 Approach:biophysical modeling· 1 Research Focus:database / resource· 1 Approach:experimental assay· 1

Frequent Co-Authors

Aaron R. HaeusleriD· 3 shared Davide TrottiiD· 2 shared Piera PasinelliiD· 2 shared Andrew T. Nelson· 1 shared Ashley V. BoehringeriD· 1 shared Giovanni ManfrediiD· 1 shared Hibiki KawamataiD· 1 shared Huan WangiD· 1 shared

Activity by Year

2024-2026 · peak 1/yr

Co-Author Collaboration Network

10 top collaborators · 24 mutual co-author links

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3 shared papersNeuroscience

Aaron R. HaeuslerORCID

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3 papers

Recent·Most cited

RNA G-Quadruplexes Function as a Tunable Switch of FUS Phase Separation

Jenny L. Carey, Miyuki Hayashi, Emily M. Welebob, Laura R. Ganser, Huan Wang, Kerry Buckhaults, Jacquelyn A. DePierro, Zheng Shi, James Shorter, Sua Myong, Aaron R. Haeusler, Lin E. Guo

This study identifies RNA G-quadruplexes as tunable regulators of FUS phase separation, showing they can inhibit or nucleate aggregation depending on structure and concentration.

Nucleic Acids Research · Jun 4, 2026Peer-reviewedBiochemistry

Neuronal Activity-Dependent Gene Dysregulation in C9orf72 i3 Neuronal Models of ALS/FTD Pathogenesis

Layla Ghaffari, Emily M. Welebob, Sarah E. Bond Newton, Ashley V. Boehringer, Kelly Cyliax, Piera Pasinelli, Davide Trotti, Aaron R. Haeusler

This study shows that C9orf72 repeat expansion neurons have altered transcriptomes under different stimulation conditions, revealing activity-dependent gene dysregulation in ALS/FTD.

American Journal of Physiology-Cell Physiology · Aug 28, 2025Peer-reviewedNeuroscience

Glucose Hypometabolism Prompts RAN Translation and Exacerbates C9orf72-related ALS/FTD Phenotypes

Andrew T. Nelson, M.E. Cicardi, Shashirekha S. Markandaiah, John Ys Han, Nancy J. Philp, Emily M. Welebob, Aaron R. Haeusler, Piera Pasinelli, Giovanni Manfredi, Hibiki Kawamata, Davide Trotti

This study shows glucose hypometabolism in C9orf72-related ALS/FTD leads to DPR production, neuronal death, and motor dysfunction through GCN2 activation.

EMBO Reports · Apr 29, 2024Peer-reviewedNeuroscience