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Christoph Bartenhagen

As seen in: British Journal of Cancer, Nature, Cell Press
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Articles

Author Correction: Ribosomal modifications are associated with mesenchymal fate selection in the neural crest lineage

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By Irina Poverennaya, Aliia Murtazina, Lei Li, Lorena Maili, Lukas Sourada, Luis Fernando Montaño-Gutierrez, Tobias Steinschaden, Markéta Kaiser, Tomas Zikmund, Teng Gao, Aurore Attina, Christoph Bartenhagen, Alek G. Erickson, Shiyuan Chen, Kristyna Polaskova, Jaroslav Sterba, Emma Andersson, Varsha Prakash, Theresa Nithila Vincent, Maria E. Arceo, María Dolores Arceo, Per Kogner, Susanne Schlisio, Peter V. Kharchenko, Alexandre Frayze David, Jozef Kaiser, Matthias Fischer Verified, Jan Skoda, Paul Trainor, Andrei S Chagin, Igor Adameyko, Rozalina Galimullina, Adna Goralija, Ornella Clara, Yaakov Gershtein, Bettina Semsch
| Nature Verified
Correction to: Nature Communications https://doi.org/10.1038/s41467-026-70375-6, published online 9 March 2026 In the version of this article initially published, the surname of Bettina Semsch was misspelled (Semasch), the surname of Emma R. Andersson was misspelled (Anderson), and the middle name initial of Alek G. Erickson was missing. The names have been amended in the HTML and PDF versions of the article.
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Centromeric footprints preserve telomere integrity in ALT cancers

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By Ragini Bhargava, Megan A Mahlke, Tobias Schmidt, Christoph Bartenhagen, Baylee Smith, Katherine Ramsey, Michelle L. Lynskey, Anne R. Wondisford, Michael Calderon, Simon Watkins Verified, Jennifer Bone, Alok Joglekar, Matthias Fischer Verified, Jan Karlseder, Yael Nechemia-Arbely, Roderick J. O’Sullivan, Takoda T. Zuehlke, Ray W. Bowman II, Jean-Baptiste Ouriou, Sandra Schamus-Hayes, April E. Williams-Wehner
| Nature Verified
Abstract Alternative lengthening of telomeres (ALT) is a specialized telomere extension mechanism associated with 5–10% of all cancers1. Although ALT has been linked to epigenetic dysregulation and genome instability, specific genomic and epigenetic rearrangements generated after ALT activation have not been identified.
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PRDX6 contributes to selenocysteine metabolism and ferroptosis resistance

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By Zhiyi Chen, Alex Inague, Kamini Kaushal, Gholamreza Fazeli, Tasneem Cheytan, Florencio Porto Freitas, Umut Yildiz, Lucas Gasparello Viviani, Rodrigo Lima, Mikaela Peglow Pinz, Thais Satie Iijima, Larissa Diniz, Judith Klein-Seetharaman, Andreas Trumpp, Adriana Mañas, Robert J. Hondal, Christoph Bartenhagen, Matthias Fischer Verified, Briana K. Shimada, Thilo Samson Chillon, Marietta Fabiano, Lutz Schomburg, Ulrich E. Schweizer, Flavia C. Meotti, Tobias P. Dick, Hamed Alborzinia, Sayuri Miyamoto, Danny Schilling, Isadora Medeiros, Simon Weinzweig, Lucia A. Seale, Luis E. Netto
| Cell Press Verified
Keywords ferroptosis cancer metabolism selenium selenocysteine metabolism cell death neuroblastoma Introduction Ferroptosis is a non-apoptotic form of cell death characterized by the iron-dependent accumulation of phospholipid hydroperoxides, ultimately leading to membrane rupture and cell death.1 Due to its association with various pathological conditions, including cancer, neurodegeneration, and tissue damage,2 the mechanisms regulating ferroptosis have garnered increasing interest.
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