Author

Macarena Moronta Gines

Erasmus MC

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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Molecular Biology· 2

Signature Assays, Organisms & Methods

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Approach:experimental assay· 2 Organism:human· 2 Research Focus:cell-cell communication· 1 Assay:CRISPR screen· 1 Research Focus:differential expression· 1 Research Focus:gene regulatory network inference· 1 Research Focus:variant calling· 1

Frequent Co-Authors

Kerstin S. WendtiD· 2 shared Anisha R. Ramadhin· 1 shared Beatriz PuisaciD· 1 shared Elisabeth GrafiD· 1 shared Erwan WatriniD· 1 shared Eskeatnaf MulugetaiD· 1 shared Farah DiabiD· 1 shared Feliciano J. RamosiD· 1 shared

Activity by Year

2020-2023 · peak 1/yr

Co-Author Collaboration Network

10 top collaborators · 31 mutual co-author links

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2 shared papersMolecular Biology

Kerstin S. WendtORCID

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2 papers

Recent·Most cited

CRISPR screens in sister chromatid cohesion defective cells reveal PAXIP1-PAGR1 as regulator of chromatin association of cohesin

Janne J. M. van Schie, Klaas de Lint, Thom M. Molenaar, Macarena Moronta Gines, Jesper A. Balk, Martin A. Rooimans, Khashayar Roohollahi, Govind M. Pai, Lauri Borghuis, Anisha R. Ramadhin, Francesco Corazza, Josephine C. Dorsman, Kerstin S. Wendt, Rob M.F. Wolthuis, Job de Lange

The paper identifies PAXIP1-PAGR1 as a novel cohesin regulator through CRISPR screens in cohesion defective cells, showing its role in chromatin association of cohesin independent of DNA replication.

Nucleic Acids Research · Sep 13, 2023Peer-reviewedMolecular Biology

MAU2 and NIPBL variants in Cornelia de Lange syndrome reveal MAU2-independent loading of cohesin and uncover a protective mechanism against early truncating mutations in NIPBL

Ilaria Parenti, Farah Diab, Sara Ruiz Gil, Eskeatnaf Mulugeta, Valentina Casà, Riccardo Berutti, Rutger W. W. Brouwer, Valérie Dupé, Juliane Eckhold, Elisabeth Graf, Beatriz Puisac, Feliciano J. Ramos, Thomas Schwarzmayr, Macarena Moronta Gines, Thomas van Staveren, , Kerstin S. Wendt

The paper investigates variants in MAU2 and NIPBL in CdLS, showing NIPBL haploinsufficiency as the main cause and revealing a protective mechanism for NIPBL out-of-frame mutations.

Cell Reports · May 1, 2020Peer-reviewedMolecular Biology