Author

G. M. Bidgood

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· 2

Signature Assays, Organisms & Methods

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Approach:experimental assay· 2 Organism:mouse· 2 Research Focus:cancer & tumor microenvironment· 1 Research Focus:cell signaling & trafficking· 1 Research Focus:development & morphogenesis· 1 Research Focus:host-pathogen & immune response· 1

Frequent Co-Authors

E. Leong· 2 shared A. Kueh· 1 shared C. D. Hyland· 1 shared F. Dehkhoda· 1 shared J. J. Babon· 1 shared J. Rautela· 1 shared J. Vince· 1 shared K. Doggett· 1 shared

Activity by Year

2022-2023 · peak 1/yr

Co-Author Collaboration Network

10 top collaborators · 25 mutual co-author links

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2 shared papersCell Biology

E. Leong

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2 papers

Recent·Most cited

CD45 limits Natural Killer cell development from common lymphoid progenitors

L. G. Meza Guzman, C. D. Hyland, G. M. Bidgood, E. Leong, Z. Shen, W. Goh, T. Kratina, J. Rautela, J. Vince, S. Nicholson, N. Huntington

This study shows that CD45 deficiency in common lymphoid progenitors causes NK cell developmental defects, not enhanced persistence, suggesting CD45 inhibition could improve in vitro NK cell generation for therapy.

bioRxiv · Apr 17, 2023 · PreprintCell Biology

The SOCS1 KIR and SH2 domain are both required for suppression of cytokine signaling in vivo

K. Doggett, N. Keating, F. Dehkhoda, G. M. Bidgood, E. Leong, A. Kueh, N. A. Nicola, N. J. Kershaw, J. J. Babon, W. S. Alexander, S. E. Nicholson

This study shows that both the KIR and SH2 domains of SOCS1 are essential for its function in suppressing cytokine signaling, as mutations in either domain lead to neonatal lethality and inflammation.

bioRxiv · Dec 20, 2022 · PreprintCell Biology