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7 results on '"Löber, Jens"'

2. Transcription factor EB sets the stage for fate decisions of antigen-primed B cells in the absence and presence of co-stimulation

Author

Wienands, Jürgen, primary, Münchhalfen, Matthias, additional, Görg, Richard, additional, Löber, Jens, additional, Willenbrink, Jakob, additional, Schwarzt, Laura, additional, Höltermann, Charlotte, additional, Chapuy, Björn, additional, Ickes, Christian, additional, Kus, Jan, additional, and Engels, Niklas, additional

Published
2022
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3. Activated SUMOylation restricts MHC class I antigen presentation to confer immune evasion in cancer

Author

Demel, Uta M., Böger, Marlitt, Yousefian, Schayan, Grunert, Corinna, Zhang, Le, Hotz, Paul W., Gottschlich, Adrian, Köse, Hazal, Isaakidis, Konstandina, Vonficht, Dominik, Grünschläger, Florian, Rohleder, Elena, Wagner, Kristina, Dönig, Judith, Igl, Veronika, Brzezicha, Bernadette, Baumgartner, Francis, Habringer, Stefan, Löber, Jens, Chapuy, Björn, Weidinger, Carl Thomas Maximilian, Kobold, Sebastian, Haas, Simon, Busse, Antonia B., Müller, Stefan, Wirth, Matthias, Schick, Markus, Keller, Ulrich, Demel, Uta M., Böger, Marlitt, Yousefian, Schayan, Grunert, Corinna, Zhang, Le, Hotz, Paul W., Gottschlich, Adrian, Köse, Hazal, Isaakidis, Konstandina, Vonficht, Dominik, Grünschläger, Florian, Rohleder, Elena, Wagner, Kristina, Dönig, Judith, Igl, Veronika, Brzezicha, Bernadette, Baumgartner, Francis, Habringer, Stefan, Löber, Jens, Chapuy, Björn, Weidinger, Carl Thomas Maximilian, Kobold, Sebastian, Haas, Simon, Busse, Antonia B., Müller, Stefan, Wirth, Matthias, Schick, Markus, and Keller, Ulrich

Abstract

Activated SUMOylation is a hallmark of cancer. Starting from a targeted screening for SUMO-regulated immune evasion mechanisms, we identified an evolutionarily conserved function of activated SUMOylation, which attenuated the immunogenicity of tumor cells. Activated SUMOylation allowed cancer cells to evade CD8+ T cell–mediated immunosurveillance by suppressing the MHC class I (MHC-I) antigen-processing and presentation machinery (APM). Loss of the MHC-I APM is a frequent cause of resistance to cancer immunotherapies, and the pharmacological inhibition of SUMOylation (SUMOi) resulted in reduced activity of the transcriptional repressor scaffold attachment factor B (SAFB) and induction of the MHC-I APM. Consequently, SUMOi enhanced the presentation of antigens and the susceptibility of tumor cells to CD8+ T cell–mediated killing. Importantly, SUMOi also triggered the activation of CD8+ T cells and thereby drove a feed-forward loop amplifying the specific antitumor immune response. In summary, we showed that activated SUMOylation allowed tumor cells to evade antitumor immunosurveillance, and we have expanded the understanding of SUMOi as a rational therapeutic strategy for enhancing the efficacy of cancer immunotherapies.

Published
2022

4. Activated SUMOylation restricts MHC class I antigen presentation to confer immune evasion in cancer

Author

Demel, Uta M., primary, Böger, Marlitt, additional, Yousefian, Schayan, additional, Grunert, Corinna, additional, Zhang, Le, additional, Hotz, Paul W., additional, Gottschlich, Adrian, additional, Köse, Hazal, additional, Isaakidis, Konstandina, additional, Vonficht, Dominik, additional, Grünschläger, Florian, additional, Rohleder, Elena, additional, Wagner, Kristina, additional, Dönig, Judith, additional, Igl, Veronika, additional, Brzezicha, Bernadette, additional, Baumgartner, Francis, additional, Habringer, Stefan, additional, Löber, Jens, additional, Chapuy, Björn, additional, Weidinger, Carl, additional, Kobold, Sebastian, additional, Haas, Simon, additional, Busse, Antonia B., additional, Müller, Stefan, additional, Wirth, Matthias, additional, Schick, Markus, additional, and Keller, Ulrich, additional

Published
2022
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5. The proteogenomic subtypes of acute myeloid leukemia

Author

Jayavelu, Ashok Kumar, primary, Wolf, Sebastian, additional, Buettner, Florian, additional, Alexe, Gabriela, additional, Häupl, Björn, additional, Comoglio, Federico, additional, Schneider, Constanze, additional, Doebele, Carmen, additional, Fuhrmann, Dominik C., additional, Wagner, Sebastian, additional, Donato, Elisa, additional, Andresen, Carolin, additional, Wilke, Anne C., additional, Zindel, Alena, additional, Jahn, Dominique, additional, Splettstoesser, Bianca, additional, Plessmann, Uwe, additional, Münch, Silvia, additional, Abou-El-Ardat, Khali, additional, Makowka, Philipp, additional, Acker, Fabian, additional, Enssle, Julius C., additional, Cremer, Anjali, additional, Schnütgen, Frank, additional, Kurrle, Nina, additional, Chapuy, Björn, additional, Löber, Jens, additional, Hartmann, Sylvia, additional, Wild, Peter J., additional, Wittig, Ilka, additional, Hübschmann, Daniel, additional, Kaderali, Lars, additional, Cox, Jürgen, additional, Brüne, Bernhard, additional, Röllig, Christoph, additional, Thiede, Christian, additional, Steffen, Björn, additional, Bornhäuser, Martin, additional, Trumpp, Andreas, additional, Urlaub, Henning, additional, Stegmaier, Kimberly, additional, Serve, Hubert, additional, Mann, Matthias, additional, and Oellerich, Thomas, additional

Published
2022
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7. SH2 domain-containing inositol 5-phosphatases support the survival of Burkitt lymphoma cells by promoting energy metabolism.

Author

Mayr F, Kruse V, Fuhrmann DC, Wolf S, Löber J, Alsouri S, Paglilla N, Lee K, Chapuy B, Brüne B, Zenz T, Häupl B, Oellerich T, and Engelke M

Subjects
Humans, Cell Line, Tumor, Apoptosis, src Homology Domains, Signal Transduction, Cell Proliferation, Receptors, Antigen, B-Cell metabolism, Burkitt Lymphoma metabolism, Burkitt Lymphoma genetics, Burkitt Lymphoma pathology, Energy Metabolism, Phosphatidylinositol-3,4,5-Trisphosphate 5-Phosphatases metabolism, Phosphatidylinositol-3,4,5-Trisphosphate 5-Phosphatases genetics, Cell Survival
Abstract

Burkitt lymphoma cells (BL) exploit antigen-independent tonic signals transduced by the B-cell antigen receptor (BCR) for their survival, but the molecular details of the rewired BL-specific BCR signal network remain unclear. A loss of function screen revealed the SH2 domain-containing 5`-inositol phosphatase 2 (SHIP2) as a potential modulator of BL fitness. We characterized the role of SHIP2 in BL survival in several BL cell models and show that perturbing SHIP2 function renders cells more susceptible to apoptosis, while attenuating proliferation in a BCR-dependent manner. Unexpectedly, SHIP2 deficiency did neither affect PI3K survival signals nor MAPK activity, but attenuated ATP production. We found that an efficient energy metabolism in BL cells requires phosphatidylinositol-3,4-bisphosphate (PI(3,4)P2), which is the enzymatic product of SHIP proteins. Consistently, interference with the function of SHIP1 and SHIP2 augments BL cell susceptibility to PI3K inhibition. Notably, we provide here a molecular basis of how tonic BCR signals are connected to energy supply, which is particularly important for such an aggressively growing neoplasia. These findings may help to improve therapies for the treatment of BL by limiting energy metabolism through the inhibition of SHIP proteins, which renders BL cells more susceptible to the targeting of survival signals.

Published
2024
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