Author

Stefanie Koidl

University of Freiburg

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 Cancer Biology· 1

Signature Assays, Organisms & Methods

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Organism:human· 3 Approach:statistical model· 3 Assay:proteomics· 2 Assay:bulk RNA-seq· 1 Research Focus:cell-cell communication· 1 Research Focus:differential expression· 1 Research Focus:gene regulatory network inference· 1

Frequent Co-Authors

Sheikh NizamuddiniD· 3 shared H. T. Marc TimmersiD· 2 shared Martin Lothar Biniossek· 2 shared Andrea PrunottoiD· 1 shared Bettina Liebowitz Knapp· 1 shared Carsten SchwaniD· 1 shared Ewoud J. van der Lelij· 1 shared Ezgi Ozyerli‐GoknariD· 1 shared

Activity by Year

2022-2026 · peak 1/yr

Co-Author Collaboration Network

10 top collaborators · 29 mutual co-author links

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3 shared papersMolecular Biology

Sheikh NizamuddinORCID

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Author profile →

3 papers

Recent·Most cited

SMAD4 MH2 Mutations Disrupt CREBBP/EP300 Recruitment and TGF-β-Induced Transcription in Colorectal Cancer

Md Saiful Islam, Sheikh Nizamuddin, Timothy En Haw Chan, Omid Fotouhi, Stefanie Koidl, H. T. Marc Timmers

This study shows that SMAD4 MH2 mutations in colorectal cancer impair CREBBP/EP300 recruitment and TGF-β-induced transcription, explaining their loss-of-function effects.

bioRxiv · Jul 1, 2026 · PreprintCancer Biology

TAF2 condensation in nuclear speckles links basal transcription factor TFIID to RNA splicing

Tanja Bhuiyan, Niccolò Arecco, Paulina Karen Mendoza Sanchez, Juhyeong Kim, Carsten Schwan, Sophie Weyrauch, Sheikh Nizamuddin, Andrea Prunotto, Mehmet Tekman, Martin Lothar Biniossek, Bettina Liebowitz Knapp, Stefanie Koidl, Friedel Drepper, Pitter F. Huesgen, Robert Grosse, , Sebastian J. Arnold

This study shows TAF2's intrinsically disordered region drives condensation in nuclear speckles, recruiting SRRM2 to TFIID and affecting alternative splicing.

Cell Reports · Apr 25, 2025Peer-reviewedMolecular Biology

Multi-omics analyses of MEN1 missense mutations identify disruption of menin-MLL and menin-JunD interactions as critical requirements for molecular pathogenicity

Koen M.A. Dreijerink, Ezgi Ozyerli‐Goknar, Stefanie Koidl, Ewoud J. van der Lelij, Priscilla van den Heuvel, Jeffrey J. Kooijman, Martin Lothar Biniossek, Kees W. Rodenburg, Sheikh Nizamuddin, H. T. Marc Timmers

The paper identifies MEN1 missense mutations that disrupt menin-MLL and menin-JunD interactions, highlighting their role in pathogenicity.

Epigenetics & Chromatin · Aug 8, 2022Peer-reviewedMolecular Biology