Author

H. Vos

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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Biochemistry· 1 Cancer Biology· 1 Immunology· 1

Signature Assays, Organisms & Methods

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Approach:experimental assay· 2 Organism:human· 2 Research Focus:cell type annotation· 1 Research Focus:clustering· 1 Approach:deep learning· 1 Research Focus:differential expression· 1 Research Focus:drug response / drug discovery· 1 Research Focus:host-pathogen & immune response· 1

Frequent Co-Authors

A. Antoranz· 1 shared A. Bassez· 1 shared A. Franken· 1 shared A. Smeets· 1 shared B. Boeckx· 1 shared B. M. Burgering· 1 shared B. Reif· 1 shared B. Thienpont· 1 shared

Activity by Year

2019-2022 · peak 1/yr

Co-Author Collaboration Network

10 top collaborators · 22 mutual co-author links

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1 shared paperCancer Biology

A. Antoranz

Mutual co-authors in cluster

Author profile →

3 papers

Recent·Most cited

Hsa-miR-31-5p controls a metabolic switch in psoriatic keratinocytes that identifies therapeutic intervention

M. Wang, Y. Yong, H. Vos, M. C. Gulersonmez, E. C. A. Stigter, J. Gerrits, M. Pages Gallego, R. van Es, L. Li, H. Deng, L. Han, R. Huang, C. Lu, B. M. Burgering

This study shows that miR-31-5p in psoriatic keratinocytes promotes a metabolic switch to glutamine metabolism, leading to immune-modulatory effects and Th17 cell differentiation, which can be inhibited by GLS targeting.

bioRxiv · Jan 21, 2022 · PreprintImmunology

A Pan-Cancer Blueprint of the Heterogeneous Tumour Microenvironment Revealed by Single-Cell Profiling

J. Qian, S. Olbrecht, B. Boeckx, H. Vos, D. Laoui, E. Etlioglu, E. Wauters, V. Pomella, S. Verbandt, P. Busschaert, A. Bassez, A. Franken, M. Vanden Bempt, J. Xiong, B. Weynand, , D. Lambrechts

This study profiles single cells from multiple cancer types to create a pan-cancer blueprint of stromal cell heterogeneity, identifying shared and unique cell populations and their characteristics.

bioRxiv · Apr 1, 2020Cancer Biology

Cysteine oxidation triggers amyloid fibril formation of the tumor suppressor p16INK4A

C. Goebl, V. Morris, L. van Dam, M. Visscher, P. Polderman, C. Hartlmueller, H. de Ruiter, M. Hora, L. Liesinger, R. Birner-Gruenberger, H. Vos, B. Reif, T. Madl, T. Dansen

This study shows that cysteine oxidation in p16INK4A leads to amyloid fibril formation, which inactivates its tumor suppressor function.

bioRxiv · Jan 2, 2019Biochemistry