Author

S. Blaser

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 Ecology· 1 Microbiology· 1

Signature Assays, Organisms & Methods

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Approach:experimental assay· 2 Research Focus:cell type annotation· 1 Research Focus:development & morphogenesis· 1 Research Focus:differential expression· 1 Research Focus:gene regulatory network inference· 1 Approach:genetic perturbation / CRISPR· 1 Research Focus:host-pathogen & immune response· 1 Organism:human· 1

Frequent Co-Authors

A. Fasano· 1 shared A. Hammond· 1 shared A. M. Lozano· 1 shared A. Sanchez· 1 shared B. Ruffner· 1 shared C. Burns· 1 shared C. S. Asensio· 1 shared C. Sepulveda· 1 shared

Activity by Year

2018-2023 · peak 1/yr

Co-Author Collaboration Network

10 top collaborators · 22 mutual co-author links

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1 shared paperCell Biology

A. Fasano

Mutual co-authors in cluster

Author profile →

3 papers

Recent·Most cited

Distribution of the invasive Anisandrus maiche (Coleoptera: Scolytinae) in Switzerland, first record in Europe of its ambrosia fungus Ambrosiella cleistominuta, and its new association with Xylosandrus crassiusculus

J. P. Ribeiro-Correia, S. Prospero, L. Beenken, P. H. W. Biedermann, S. Blaser, Y. Chittaro, D. Frey, D. Hölling, S. O. Kaya, M. Knizek, J. Mittelstrass, M. Branco, B. Ruffner, A. Sanchez, E. G. Brockerhoff

bioRxiv · Mar 30, 2023 · PreprintEcology

VPS41 recessive mutation causes ataxia and dystonia with retinal dystrophy and mental retardation by inhibiting HOPS function and mTORC1 signaling

R. E. N. van der Welle, R. Jobling, C. Burns, P. Sanza, C. ten Brink, A. Fasano, L. Chen, F. J. Zwartkruis, S. Zwakenberg, E. F. Griffin, J. van der Beek, T. Veenendaal, N. Liv, S. Blaser, C. Sepulveda, , J. Klumperman

This paper identifies VPS41 mutations causing neurodegenerative disease by disrupting HOPS function and mTORC1 signaling, leading to lysosomal dysfunction and impaired autophagy.

bioRxiv · Dec 18, 2019 · PreprintCell Biology

An infant mouse model of influenza virus transmission demonstrates the role of virus-specific shedding, humoral immunity, and sialidase expression by colonizing Streptococcus pneumoniae.

M. B. Ortigoza, S. Blaser, M. A. Zafar, A. Hammond, J. N. Weiser

This paper introduces an infant mouse model to study influenza virus transmission, showing that viral shedding, age, humoral immunity, and sialidase activity of Streptococcus pneumoniae influence transmission efficiency.

bioRxiv · Oct 31, 2018Microbiology