Author

Thomas Fath

Macquarie UniversityORCID 0000-0002-6877-7567Unclaimed ORCID profile · follow to get notified of new preprints

Biology Disciplines

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Signature Assays, Organisms & Methods

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Approach:experimental assay· 4 Organism:mouse· 4 Research Focus:cell signaling & trafficking· 1 Research Focus:cell type annotation· 1 Research Focus:differential expression· 1 Research Focus:drug response / drug discovery· 1 Assay:electronic health records· 1 Assay:fluorescence / live-cell microscopy· 1

Frequent Co-Authors

Holly StefeniD· 3 shared Edna C. HardemaniD· 2 shared Esmeralda ParićiD· 2 shared Peter William GunningiD· 2 shared Tamara TomanićiD· 2 shared A. ChieniD· 1 shared Alexandra K. SuchowerskaiD· 1 shared Amr AbouelezziD· 1 shared

Activity by Year

2020-2025 · peak 2/yr

Co-Author Collaboration Network

10 top collaborators · 25 mutual co-author links

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Curved chords = mutual co-authorship

3 shared papersNeuroscience

Holly StefenORCID

Mutual co-authors in cluster

Author profile →

4 papers

Recent·Most cited

Knock-out of Tpm4.2/actin filaments alters neuronal signaling, neurite outgrowth and behavioral phenotypes in mice.

Sian Genoud, Chanchanok Chaichim, Rossana Rosa Porto, Tamara Tomanić, Holly Stefen, Esmeralda Parić, Soumalya Sarkar, Dasol Yoo, Wendi Gao, Edna C. Hardeman, Peter William Gunning, Tim Karl, John Power, Thomas Fath

This study investigates the role of Tpm4.2 in neuronal processes by analyzing knock-out mice, finding altered signaling, neurite outgrowth, and sex-dependent behavioral phenotypes.

Molecular Neurobiology · Aug 2, 2025Peer-reviewedNeuroscience

Fluorescence recovery after photobleaching reveals different 1 behaviour2 of tropomyosin isoforms Tpm3.1 and Tpm4.2 in dendritic spines

Tamara Tomanić, Holly Stefen, Esmeralda Parić, A. Chien, Thomas Fath

This study uses FRAP to show Tpm3.1 and Tpm4.2 have distinct kinetic behaviors in dendritic spines and different effects on actin turnover.

bioRxiv · Jul 22, 2025 · PreprintCell Biology

Dysregulated actin dynamics and cofilin correlate with TDP-43 pathology in sporadic amyotrophic lateral sclerosis

Cyril Jones Jagaraj, Prachi M. Mehta, Sonam Parakh, Sina Shadfar, Shafi Jamali, Alexandra K. Suchowerska, Jessica Sultana, Thomas Fath, Julie D. Atkin

This study shows that dysregulated actin dynamics and cofilin phosphorylation are linked to TDP-43 pathology in sporadic ALS, suggesting potential therapeutic targets.

bioRxiv · Aug 28, 2023 · PreprintNeuroscience

Tropomyosin Tpm3.1 is required to maintain the structure and function of the axon initial segment

Amr Abouelezz, Holly Stefen, Mikael Segerstråle, David Micinski, Rimante Minkeviciene, Lauri Lahti, Edna C. Hardeman, Peter William Gunning, Casper C. Hoogenraad, Tomi Taira, Thomas Fath, Pirta Hotulainen

This study identifies Tpm3.1 as essential for maintaining AIS structure and function by stabilizing actin filaments in the axon initial segment.

iScience · Apr 12, 2020Peer-reviewedNeuroscience