Author

M. F. Alemdehy

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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Immunology· 2 Cell Biology· 1

Signature Assays, Organisms & Methods

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Research Focus:cell type annotation· 3 Assay:ChIP-seq· 3 Research Focus:chromatin & epigenetic regulation· 3 Organism:mouse· 3 Approach:experimental assay· 2 Approach:statistical model· 2 Assay:bulk RNA-seq· 1 Research Focus:cancer & tumor microenvironment· 1

Frequent Co-Authors

F. van Leeuwen· 3 shared H. Jacobs· 3 shared C. Lancini· 2 shared C. McLean· 2 shared E. de Wit· 2 shared E. M. Kwesi-Maliepaard· 2 shared H. Vlaming· 2 shared M. A. Aslam· 2 shared

Activity by Year

2019-2020 · peak 2/yr

Co-Author Collaboration Network

10 top collaborators · 45 mutual co-author links

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3 shared papersImmunology

F. van Leeuwen

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Author profile →

3 papers

Recent·Most cited

Histone methyltransferase DOT1L controls state-specific identity during B cell differentiation

M. A. Aslam, M. F. Alemdehy, E. M. Kwesi-Maliepaard, M. Caganova, I. N. Pardieck, T. van den Brand, F. I. Muhaimi, T. van Welsem, I. de Rink, J.-Y. Song, E. de Wit, R. Arens, K. Rajewsky, H. Jacobs, F. van Leeuwen

This study identifies DOT1L as a key regulator of B cell differentiation by controlling epigenetic programs that maintain B cell naivety and support germinal center formation.

bioRxiv · Mar 25, 2020Immunology

The histone methyltransferase DOT1L prevents antigen-independent differentiation and safeguards epigenetic identity of CD8+ T cells

E. M. Kwesi-Maliepaard, M. A. Aslam, M. F. Alemdehy, T. van den Brand, C. McLean, H. Vlaming, T. van Welsem, T. Korthout, C. Lancini, S. Hendriks, T. Ahrends, D. van Dinther, J. M. den Haan, J. Borst, E. de Wit, , H. Jacobs

This study shows that DOT1L prevents premature differentiation of CD8+ T cells and maintains their epigenetic identity, independent of antigen exposure.

bioRxiv · Nov 18, 2019Immunology

Evolutionarily-conserved chromatin crosstalk generates a DOT1L-dose dependency in thymic lymphoma caused by loss of HDAC1

H. Vlaming, C. McLean, T. Korthout, M. F. Alemdehy, S. Henriks, C. Lancini, S. Palit, S. Klarenbeek, T. M. Molenaar, L. Hoekman, T. T. Schmidlin, M. Altelaar, T. v. Welsem, J.-H. Dannenberg, H. Jacobs, F. van Leeuwen

The paper identifies an evolutionarily-conserved interaction between HDAC1 and DOT1L that influences H3K79 methylation and contributes to thymic lymphoma development.

bioRxiv · Jan 10, 2019Cell Biology