Author

E. M. Hol

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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Cancer Biology· 1 Cell Biology· 1

Signature Assays, Organisms & Methods

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Research Focus:cancer & tumor microenvironment· 2 Approach:experimental assay· 2 Assay:bulk RNA-seq· 1 Research Focus:cell signaling & trafficking· 1 Research Focus:cell type annotation· 1 Research Focus:host-pathogen & immune response· 1 Organism:human· 1 Assay:imaging· 1

Frequent Co-Authors

A. S. Margarido· 1 shared C. Vennin· 1 shared E. J. van Bodegraven· 1 shared E. van Bodegraven· 1 shared J. A. Sluijs· 1 shared J. Sluijs· 1 shared J. V. van Asperen· 1 shared J. van Rheenen· 1 shared

Activity by Year

2020-2021 · peak 1/yr

Co-Author Collaboration Network

10 top collaborators · 21 mutual co-author links

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1 shared paperCell Biology

A. S. Margarido

Mutual co-authors in cluster

Author profile →

2 papers

Recent·Most cited

GFAP splice variants fine-tune glioma cell invasion and tumour dynamics by modulating migration persistence

J. V. van Asperen, R. Uceda-Castro, C. Vennin, J. Sluijs, E. J. van Bodegraven, A. S. Margarido, P. Robe, J. van Rheenen, E. M. Hol

This study shows that GFAP splice variants differentially regulate glioma cell migration and invasion, with GFAP{delta} depletion causing random migration and GFAP depletion enabling directional persistence.

bioRxiv · Aug 19, 2021Cell Biology

New GFAP splice isoform (GFAPμ) differentially expressed in glioma translates into 21 kDa N-terminal GFAP protein

E. van Bodegraven, J. A. Sluijs, K. A. Tan, P. A. J. T. Robe, E. M. Hol

The paper identifies a new GFAP splice isoform, GFAPμ, differentially expressed in glioma subtypes, which translates into a 21 kDa N-terminal GFAP protein that disrupts the GFAP intermediate filament network.

bioRxiv · Jul 4, 2020Cancer Biology