Author

H. J. Worman

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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Cell Biology· 5

Signature Assays, Organisms & Methods

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Approach:experimental assay· 4 Organism:mouse· 4 Research Focus:cell signaling & trafficking· 3 Research Focus:cell type annotation· 3 Research Focus:cancer & tumor microenvironment· 1 Research Focus:development & morphogenesis· 1 Research Focus:differential expression· 1 Assay:electronic health records· 1

Frequent Co-Authors

J.-Y. Shin· 4 shared C. Ostlund· 3 shared A. Hernandez-Ono· 2 shared H. N. Ginsberg· 2 shared W. T. Dauer· 2 shared W. Wu· 2 shared Y. Wang· 2 shared A. Shi· 1 shared

Activity by Year

2018-2023 · peak 1/yr

Co-Author Collaboration Network

10 top collaborators · 26 mutual co-author links

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4 shared papersCell Biology

J.-Y. Shin

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5 papers

Recent·Most cited

Functional interaction of torsinA and its activators in liver lipid metabolism

A. Hernandez-Ono, Y. P. Zhao, J. W. Murray, C. Ostlund, M. J. Lee, A. Shi, W. T. Dauer, H. J. Worman, H. N. Ginsberg, J.-Y. Shin

The paper shows that torsinA and its activators LAP1 and LULL1 regulate liver triglyceride secretion and steatosis in mice.

bioRxiv · Jun 21, 2023Cell Biology

Hepatocytes deficient in nuclear envelope protein lamina-associated polypeptide 1 are an ideal mammalian system to study intranuclear lipid droplets

C. Ostlund, A. Hernandez-Ono, S. J. Turk, W. T. Dauer, H. N. Ginsberg, H. J. Worman, J.-Y. Shin

This study shows that LAP1-depleted hepatocytes are an ideal system to study nuclear lipid droplets and their response to nutritional changes.

bioRxiv · Jun 27, 2022Cell Biology

Abolishing the prelamin A ZMPSTE24 cleavage site leads to progeroid phenotypes with near-normal longevity in mice

Y. Wang, K. Shiladardi, T. Hsu, K. O. Odinammadu, T. Maruyama, W. Wu, C.-S. Lin, C. B. Damoci, E. D. Spear, J.-Y. Shin, W. Hsu, S. Michaelis, H. J. Worman

This study shows that mice with permanently farnesylated prelamin A live nearly normal lifespans but show aging-related defects, suggesting prelamin A accumulation contributes to aging phenotypes.

bioRxiv · Nov 11, 2021Cell Biology

A lamin A/C variant causing striated muscle disease provides insights into filament organization

O. Medalia, R. Kronenberg-Tenga, M. Tatli, M. Eibauer, W. Wu, J.-Y. Shin, G. Bonne, H. J. Worman

This study examines a lamin A/C mutation in mice, revealing structural changes in nuclear filaments and chromatin organization linked to striated muscle disease.

bioRxiv · Oct 20, 2020Cell Biology

Imbalanced Nucleocytoskeletal Connections Create Common Polarity Defects in Progeria and Physiological Aging

W. Chang, Y. Wang, G. W. G. Luxton, C. Ostlund, H. J. Worman, G. G. Gundersen

This study identifies imbalanced nucleocytoskeletal connections as a cause of polarity defects in progeria and aging, showing that rebalancing these connections can restore normal cell function.

bioRxiv · Dec 15, 2018Cell Biology