Author

A. S. Meijers

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 Immunology· 1 Microbiology· 1

Signature Assays, Organisms & Methods

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Approach:experimental assay· 3 Organism:human· 3 Organism:mouse· 2 Research Focus:cancer & tumor microenvironment· 1 Research Focus:cell signaling & trafficking· 1 Research Focus:cell type annotation· 1 Research Focus:development & morphogenesis· 1 Research Focus:differential expression· 1

Frequent Co-Authors

A. J. Affandi· 1 shared A. L. Turner· 1 shared A. Macdonald· 1 shared A. Ottria· 1 shared A. Samson· 1 shared B. Giovannone· 1 shared C. D. James· 1 shared C. Jimenez· 1 shared

Activity by Year

2021-2024 · peak 1/yr

Co-Author Collaboration Network

10 top collaborators · 14 mutual co-author links

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1 shared paperImmunology

A. J. Affandi

Mutual co-authors in cluster

Author profile →

3 papers

Recent·Most cited

Cancer BiologybioRxivJan 8, 2024

E7-mediated repression of miR-203 promotes LASP1-dependent proliferation in HPV-positive cervical cancer

M. R. Patterson, A. S. Meijers, E. L. Ryder…·A. Macdonald

This study shows that HPV E7 represses miR-203, leading to LASP1 upregulation and promoting proliferation in HPV-positive cervical cancer.

DOI 10.1038/s41388-024-03067-4

humanexperimental assay

MicrobiologybioRxivJun 21, 2022

The ESX-1 substrate PPE68 has a key function in the ESX-1 mediated secretion in Mycobacterium marinum

M. P. M. Damen, A. S. Meijers, E. M. Keizer…·E. N. G. Houben

This paper identifies PPE68 as essential for ESX-1 mediated secretion of EsxA and EspE in M. marinum, revealing distinct domains of PPE68 involved in different secretion processes.

DOI 10.1128/mbio.02819-22

ImmunologybioRxivDec 7, 2021

Impaired LAIR-1-mediated immune control due to collagen degradation in fibrosis

T. Carvalheiro, W. Marut, M. I. Pascoal Ramos…·L. Meyaard

The paper investigates how impaired LAIR-1-collagen interaction in fibrosis contributes to inflammation and fibrosis, finding that dysfunctional collagen ligands and matrix metalloproteinases drive disease progression.

DOI 10.1016/j.jaut.2024.103219