Author

D. Maslar

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· 1 Physiology· 1

Signature Assays, Organisms & Methods

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Approach:experimental assay· 2 Research Focus:cancer & tumor microenvironment· 1 Research Focus:cell signaling & trafficking· 1 Organism:mouse· 1

Frequent Co-Authors

C. S. Asensio· 2 shared A. Rodriguez· 1 shared B. H. Hummer· 1 shared B. Yau· 1 shared C. H. Burns· 1 shared D. Chitayat· 1 shared G. W. Strout· 1 shared J. A. J. Fitzpatrick· 1 shared

Activity by Year

2019-2020 · peak 1/yr

Co-Author Collaboration Network

10 top collaborators · 37 mutual co-author links

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2 shared papersPhysiology

C. S. Asensio

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2 papers

Recent·Most cited

Pancreatic beta-cell specific deletion of VPS41 causes diabetes due to defects in insulin secretion

C. H. Burns, B. Yau, A. Rodriguez, J. D. Triplett, D. Maslar, Y. S. An, R. E. N. van der Welle, R. G. Kossina, M. R. Fisher, G. W. Strout, P. O. Bayguinov, T. Veenendaal, D. Chitayat, J. A. J. Fitzpatrick, J. Klumperman, , C. S. Asensio

This study shows that VPS41 deletion in pancreatic beta-cells causes diabetes by impairing insulin secretory granule formation and secretion.

bioRxiv · Apr 25, 2020Physiology

Differential sorting behavior for soluble and transmembrane cargoes at the trans-Golgi network in endocrine cells.

B. H. Hummer, D. Maslar, M. Soltero Gutierrez, N. F. de Leeuw, C. S. Asensio

The paper quantifies TGN budding kinetics of constitutive and regulated secretory cargoes and reveals that transmembrane cargoes exit the TGN into non-regulated vesicles before incorporation into secretory granules.

bioRxiv · Oct 8, 2019Cell Biology