Author

G. H. Su

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· 1 Physiology· 1

Signature Assays, Organisms & Methods

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Approach:experimental assay· 2 Research Focus:development & morphogenesis· 1 Research Focus:host-pathogen & immune response· 1 Organism:human· 1 Assay:imaging· 1 Organism:mouse· 1

Frequent Co-Authors

D. F. Schaeffer· 1 shared D. J. Bernard· 1 shared E. Brule· 1 shared E. R. S. Buddle· 1 shared G. Schang· 1 shared H. Schultz· 1 shared I. S. Wood· 1 shared J. L. Kopp· 1 shared

Activity by Year

2023-2023 · peak 2/yr

Co-Author Collaboration Network

10 top collaborators · 21 mutual co-author links

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1 shared paperCancer Biology

D. F. Schaeffer

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2 papers

Recent·Most cited

Myostatin is a major endocrine driver of follicle-stimulating hormone synthesis

L. Ongaro, X. Zhou, Y. Wang, Z. Zhou, H. Schultz, E. R. S. Buddle, E. Brule, Y.-F. Lin, G. Schang, R. Castonguay, Y. Liu, G. H. Su, N. Seidah, K. C. Ray, S. J. Karp, , D. J. Bernard

The paper identifies myostatin as an endocrine hormone that promotes pituitary FSH synthesis and ovarian function, challenging the previous role of activins and highlighting potential fertility risks of myostatin antagonists.

bioRxiv · Aug 30, 2023 · PreprintPhysiology

Acvr1b loss increases formation of pancreatic precancerous lesions from acinar and ductal cells of origin

K. Saeki, I. S. Wood, W. C. K. Wang, S. Patil, Y. Sun, D. F. Schaeffer, G. H. Su, J. L. Kopp

This study shows that Acvr1b loss in combination with Kras mutation promotes precancerous lesions from both acinar and ductal cells in the pancreas, but the IPMN-like phenotype differs when mutations occur in all cells.

bioRxiv · Jun 8, 2023 · PreprintCancer Biology