Author

J. R. Dobson

Listed by name: these papers carry no ORCID for this author, so different people with the same name may be mixed together.

Biology Disciplines

Click to filter author papers

Physiology· 2

Signature Assays, Organisms & Methods

Click to filter · or open tag

Research Focus:cell signaling & trafficking· 2 Assay:electrophysiology· 2 Approach:experimental assay· 2 Organism:mouse· 2 Research Focus:host-pathogen & immune response· 1 Organism:human· 1 Research Focus:metabolism & bioenergetics· 1

Frequent Co-Authors

A. Y. Nakhe· 2 shared D. A. Jacobson· 2 shared M. T. Dickerson· 2 shared P. K. Dadi· 2 shared C. F. Scott· 1 shared C. M. Schaub· 1 shared J. C. Lynch· 1 shared J. Kim· 1 shared

Activity by Year

2022-2023 · peak 1/yr

Co-Author Collaboration Network

10 top collaborators · 37 mutual co-author links

Click any collaborator node to inspect or filter shared papers

Focal author (center)Selected co-authorORCID co-authorUnlinked name

Curved chords = mutual co-authorship

2 shared papersPhysiology

A. Y. Nakhe

Mutual co-authors in cluster

Author profile →

2 papers

Recent·Most cited

The MODY-associated KCNK16 L114P mutation increases islet glucagon secretion and limits insulin secretion resulting in transient neonatal diabetes and glucose dyshomeostasis in adults

A. Y. Nakhe, P. K. Dadi, J. Kim, M. T. Dickerson, S. Behera, J. R. Dobson, S. Shrestha, J.-P. Cartailler, L. Sampson, M. A. Magnuson, D. A. Jacobson

This study shows that the KCNK16 L114P mutation causes neonatal diabetes and glucose dyshomeostasis in adult mice by disrupting islet insulin secretion and increasing glucagon secretion.

bioRxiv · Jun 20, 2023 · PreprintPhysiology

Gi/o protein-coupled receptor inhibition of beta-cell electrical excitability and insulin secretion depends on Na+/K+ ATPase activation

M. T. Dickerson, P. K. Dadi, K. E. Zaborska, A. Y. Nakhe, C. M. Schaub, J. R. Dobson, N. M. Wright, J. C. Lynch, C. F. Scott, D. A. Jacobson

This study shows that Gi/o-GPCR inhibition of beta-cell insulin secretion depends on Na+/K+ ATPase activation, which hyperpolarizes the membrane and modulates Ca2+ oscillations.

bioRxiv · Feb 10, 2022Physiology