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267 results on '"Kirchner, Marieluise"'

1. Antibodies and complement are key drivers of thrombosis

Author

Stark, Konstantin, Kilani, Badr, Stockhausen, Sven, Busse, Johanna, Schubert, Irene, Tran, Thuy-Duong, Gaertner, Florian, Leunig, Alexander, Pekayvaz, Kami, Nicolai, Leo, Fumagalli, Valeria, Stermann, Julia, Stephan, Felix, David, Christian, Müller, Martin B., Heyman, Birgitta, Lux, Anja, da Palma Guerreiro, Alexandra, Frenzel, Lukas P., Schmidt, Christoph Q., Dopler, Arthur, Moser, Markus, Chandraratne, Sue, von Brühl, Marie-Luise, Lorenz, Michael, Korff, Thomas, Rudelius, Martina, Popp, Oliver, Kirchner, Marieluise, Mertins, Philipp, Nimmerjahn, Falk, Iannacone, Matteo, Sperandio, Markus, Engelmann, Bernd, Verschoor, Admar, and Massberg, Steffen

Published
2024
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2. Frequent ZNF217 mutations lead to transcriptional deregulation of interferon signal transduction via altered chromatin accessibility in B cell lymphoma

Author

Briest, Franziska, Noerenberg, Daniel, Hennch, Cornelius, Yoshida, Kenichi, Hablesreiter, Raphael, Nimo, Jose, Sasca, Daniel, Kirchner, Marieluise, Mansouri, Larry, Inoue, Yoshikage, Wiegand, Laura, Staiger, Annette M., Casadei, Beatrice, Korkolopoulou, Penelope, Weiner, January, Lopez-Guillermo, Armando, Warth, Arne, Schneider, Tamás, Nagy, Ákos, Klapper, Wolfram, Hummel, Michael, Kanellis, George, Anagnostopoulos, Ioannis, Mertins, Philipp, Bullinger, Lars, Rosenquist, Richard, Vassilakopoulos, Theodoros P., Ott, German, Ogawa, Seishi, and Damm, Frederik

Published
2023
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4. A proteomics analysis of 5xFAD mouse brain regions reveals the lysosome-associated protein Arl8b as a candidate biomarker for Alzheimer’s disease

Author

Boeddrich, Annett, Haenig, Christian, Neuendorf, Nancy, Blanc, Eric, Ivanov, Andranik, Kirchner, Marieluise, Schleumann, Philipp, Bayraktaroğlu, Irem, Richter, Matthias, Molenda, Christine Mirjam, Sporbert, Anje, Zenkner, Martina, Schnoegl, Sigrid, Suenkel, Christin, Schneider, Luisa-Sophie, Rybak-Wolf, Agnieszka, Kochnowsky, Bianca, Byrne, Lauren M., Wild, Edward J., Nielsen, Jørgen E., Dittmar, Gunnar, Peters, Oliver, Beule, Dieter, and Wanker, Erich E.

Published
2023
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6. Evolutionary origins and interactomes of human, young microproteins and small peptides translated from short open reading frames

Author

Sandmann, Clara-L., Schulz, Jana F., Ruiz-Orera, Jorge, Kirchner, Marieluise, Ziehm, Matthias, Adami, Eleonora, Marczenke, Maike, Christ, Annabel, Liebe, Nina, Greiner, Johannes, Schoenenberger, Aaron, Muecke, Michael B., Liang, Ning, Moritz, Robert L., Sun, Zhi, Deutsch, Eric W., Gotthardt, Michael, Mudge, Jonathan M., Prensner, John R., Willnow, Thomas E., Mertins, Philipp, van Heesch, Sebastiaan, and Hubner, Norbert

Published
2023
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8. Therapeutic targeting of ATR in alveolar rhabdomyosarcoma

Author

Dorado García, Heathcliff, Pusch, Fabian, Bei, Yi, von Stebut, Jennifer, Ibáñez, Glorymar, Guillan, Kristina, Imami, Koshi, Gürgen, Dennis, Rolff, Jana, Helmsauer, Konstantin, Meyer-Liesener, Stephanie, Timme, Natalie, Bardinet, Victor, Chamorro González, Rocío, MacArthur, Ian C., Chen, Celine Y., Schulz, Joachim, Wengner, Antje M., Furth, Christian, Lala, Birgit, Eggert, Angelika, Seifert, Georg, Hundsoerfer, Patrick, Kirchner, Marieluise, Mertins, Philipp, Selbach, Matthias, Lissat, Andrej, Dubois, Frank, Horst, David, Schulte, Johannes H., Spuler, Simone, You, Daoqi, Dela Cruz, Filemon, Kung, Andrew L., Haase, Kerstin, DiVirgilio, Michela, Scheer, Monika, Ortiz, Michael V., and Henssen, Anton G.

Published
2022
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10. Protective immune trajectories in early viral containment of non-pneumonic SARS-CoV-2 infection

Author

Pekayvaz, Kami, Leunig, Alexander, Kaiser, Rainer, Joppich, Markus, Brambs, Sophia, Janjic, Aleksandar, Popp, Oliver, Nixdorf, Daniel, Fumagalli, Valeria, Schmidt, Nora, Polewka, Vivien, Anjum, Afra, Knottenberg, Viktoria, Eivers, Luke, Wange, Lucas E., Gold, Christoph, Kirchner, Marieluise, Muenchhoff, Maximilian, Hellmuth, Johannes C., Scherer, Clemens, Rubio-Acero, Raquel, Eser, Tabea, Deák, Flora, Puchinger, Kerstin, Kuhl, Niklas, Linder, Andreas, Saar, Kathrin, Tomas, Lukas, Schulz, Christian, Wieser, Andreas, Enard, Wolfgang, Kroidl, Inge, Geldmacher, Christof, von Bergwelt-Baildon, Michael, Keppler, Oliver T., Munschauer, Mathias, Iannacone, Matteo, Zimmer, Ralf, Mertins, Philipp, Hubner, Norbert, Hoelscher, Michael, Massberg, Steffen, Stark, Konstantin, and Nicolai, Leo

Published
2022
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11. Quantitative modeling of signaling in aggressive B cell lymphoma unveils conserved core network.

Author

Klinger, Bertram, Rausch, Isabel, Sieber, Anja, Kutz, Helmut, Kruse, Vanessa, Kirchner, Marieluise, Mertins, Philipp, Kieser, Arnd, Blüthgen, Nils, and Kube, Dieter

Subjects
DIFFUSE large B-cell lymphomas, B cell lymphoma, MITOGEN-activated protein kinases, B cells, CELL receptors
Abstract

B cell receptor (BCR) signaling is required for the survival and maturation of B cells and is deregulated in B cell lymphomas. While proximal BCR signaling is well studied, little is known about the crosstalk of downstream effector pathways, and a comprehensive quantitative network analysis of BCR signaling is missing. Here, we semi-quantitatively modelled BCR signaling in Burkitt lymphoma (BL) cells using systematically perturbed phosphorylation data of BL-2 and BL-41 cells. The models unveiled feedback and crosstalk structures in the BCR signaling network, including a negative crosstalk from p38 to MEK/ERK. The relevance of the crosstalk was verified for BCR and CD40 signaling in different BL cells and confirmed by global phosphoproteomics on ERK itself and known ERK target sites. Compared to the starting network, the trained network for BL-2 cells was better transferable to BL-41 cells. Moreover, the BL-2 network was also suited to model BCR signaling in Diffuse large B cell lymphoma cells lines with aberrant BCR signaling (HBL-1, OCI-LY3), indicating that BCR aberration does not cause a major downstream rewiring. Author summary: B cell receptors bind specific antigens, and upon binding, they activate a signal transduction network which ultimately primes the cells for proliferation and affinity maturation. B-cell receptor signaling is often altered in B-cell lymphoma, leading to altered or chronic activation of the network. In this study we compared the signal transduction network downstream of acute and aberrant B cell receptor activity in cell lines originating from Burkitt and diffuse large B-cell lymphoma, respectively. By applying kinase inhibitors, we measured phosphorylation state changes in the network nodes. Mathematical modeling revealed a 16-node core network conserved in cells with acute and abberant B cell receptor signaling. In the network we detected hitherto undescribed crosstalks and feedbacks, structures known to confer treatment robustness. We elucidated and verified a negative crosstalk between the mitogen-activated protein kinases (MAPK) p38 and ERK. We further discovered that the negative feedback from ERK to its upstream kinase RAF, which in solid tumors neutralizes treatments targeting ERK or MEK, is also present in B cells. Altogether these findings may inform future treatment strategies targeting overactive B cell receptor or help to explain treatment resistance. [ABSTRACT FROM AUTHOR]

Published
2024
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13. Phosphorylation of PLPPR3 membrane proteins as signaling integrator at neuronal synapses

Author

Kroon, Cristina, primary, Bareesel, Shannon, additional, Kirchner, Marieluise, additional, Gimber, Niclas, additional, Ranti, Dimitra, additional, Brosig, Annika, additional, Textoris-Taube, Kathrin, additional, Zolnik, Timothy A., additional, Mertins, Philipp, additional, Schmoranzer, Jan, additional, Leondaritis, George, additional, and Eickholt, Britta J., additional

Published
2024
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14. Supplementary Table S5 from Passenger Gene Coamplifications Create Collateral Therapeutic Vulnerabilities in Cancer

Author

Bei, Yi, primary, Bramé, Luca, primary, Kirchner, Marieluise, primary, Fritsche-Guenther, Raphaela, primary, Kunz, Severine, primary, Bhattacharya, Animesh, primary, Rusu, Mara-Camelia, primary, Gürgen, Dennis, primary, Dubios, Frank P.B., primary, Köppke, Julia K.C., primary, Proba, Jutta, primary, Wittstruck, Nadine, primary, Sidorova, Olga Alexandra, primary, Chamorro González, Rocío, primary, Dorado Garcia, Heathcliff, primary, Brückner, Lotte, primary, Xu, Robin, primary, Giurgiu, Mădălina, primary, Rodriguez-Fos, Elias, primary, Yu, Qinghao, primary, Spanjaard, Bastiaan, primary, Koche, Richard P., primary, Schmitt, Clemens A., primary, Schulte, Johannes H., primary, Eggert, Angelika, primary, Haase, Kerstin, primary, Kirwan, Jennifer, primary, Hagemann, Anja I.H., primary, Mertins, Philipp, primary, Dörr, Jan R., primary, and Henssen, Anton G., primary

Published
2024
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15. Supplementary Figures S1-S9 from Passenger Gene Coamplifications Create Collateral Therapeutic Vulnerabilities in Cancer

Author

Bei, Yi, primary, Bramé, Luca, primary, Kirchner, Marieluise, primary, Fritsche-Guenther, Raphaela, primary, Kunz, Severine, primary, Bhattacharya, Animesh, primary, Rusu, Mara-Camelia, primary, Gürgen, Dennis, primary, Dubios, Frank P.B., primary, Köppke, Julia K.C., primary, Proba, Jutta, primary, Wittstruck, Nadine, primary, Sidorova, Olga Alexandra, primary, Chamorro González, Rocío, primary, Dorado Garcia, Heathcliff, primary, Brückner, Lotte, primary, Xu, Robin, primary, Giurgiu, Mădălina, primary, Rodriguez-Fos, Elias, primary, Yu, Qinghao, primary, Spanjaard, Bastiaan, primary, Koche, Richard P., primary, Schmitt, Clemens A., primary, Schulte, Johannes H., primary, Eggert, Angelika, primary, Haase, Kerstin, primary, Kirwan, Jennifer, primary, Hagemann, Anja I.H., primary, Mertins, Philipp, primary, Dörr, Jan R., primary, and Henssen, Anton G., primary

Published
2024
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16. Data from Passenger Gene Coamplifications Create Collateral Therapeutic Vulnerabilities in Cancer

Author

Bei, Yi, primary, Bramé, Luca, primary, Kirchner, Marieluise, primary, Fritsche-Guenther, Raphaela, primary, Kunz, Severine, primary, Bhattacharya, Animesh, primary, Rusu, Mara-Camelia, primary, Gürgen, Dennis, primary, Dubios, Frank P.B., primary, Köppke, Julia K.C., primary, Proba, Jutta, primary, Wittstruck, Nadine, primary, Sidorova, Olga Alexandra, primary, Chamorro González, Rocío, primary, Dorado Garcia, Heathcliff, primary, Brückner, Lotte, primary, Xu, Robin, primary, Giurgiu, Mădălina, primary, Rodriguez-Fos, Elias, primary, Yu, Qinghao, primary, Spanjaard, Bastiaan, primary, Koche, Richard P., primary, Schmitt, Clemens A., primary, Schulte, Johannes H., primary, Eggert, Angelika, primary, Haase, Kerstin, primary, Kirwan, Jennifer, primary, Hagemann, Anja I.H., primary, Mertins, Philipp, primary, Dörr, Jan R., primary, and Henssen, Anton G., primary

Published
2024
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17. Figure 6 from Passenger Gene Coamplifications Create Collateral Therapeutic Vulnerabilities in Cancer

Author

Bei, Yi, primary, Bramé, Luca, primary, Kirchner, Marieluise, primary, Fritsche-Guenther, Raphaela, primary, Kunz, Severine, primary, Bhattacharya, Animesh, primary, Rusu, Mara-Camelia, primary, Gürgen, Dennis, primary, Dubios, Frank P.B., primary, Köppke, Julia K.C., primary, Proba, Jutta, primary, Wittstruck, Nadine, primary, Sidorova, Olga Alexandra, primary, Chamorro González, Rocío, primary, Dorado Garcia, Heathcliff, primary, Brückner, Lotte, primary, Xu, Robin, primary, Giurgiu, Mădălina, primary, Rodriguez-Fos, Elias, primary, Yu, Qinghao, primary, Spanjaard, Bastiaan, primary, Koche, Richard P., primary, Schmitt, Clemens A., primary, Schulte, Johannes H., primary, Eggert, Angelika, primary, Haase, Kerstin, primary, Kirwan, Jennifer, primary, Hagemann, Anja I.H., primary, Mertins, Philipp, primary, Dörr, Jan R., primary, and Henssen, Anton G., primary

Published
2024
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18. Figure 4 from Passenger Gene Coamplifications Create Collateral Therapeutic Vulnerabilities in Cancer

Author

Bei, Yi, primary, Bramé, Luca, primary, Kirchner, Marieluise, primary, Fritsche-Guenther, Raphaela, primary, Kunz, Severine, primary, Bhattacharya, Animesh, primary, Rusu, Mara-Camelia, primary, Gürgen, Dennis, primary, Dubios, Frank P.B., primary, Köppke, Julia K.C., primary, Proba, Jutta, primary, Wittstruck, Nadine, primary, Sidorova, Olga Alexandra, primary, Chamorro González, Rocío, primary, Dorado Garcia, Heathcliff, primary, Brückner, Lotte, primary, Xu, Robin, primary, Giurgiu, Mădălina, primary, Rodriguez-Fos, Elias, primary, Yu, Qinghao, primary, Spanjaard, Bastiaan, primary, Koche, Richard P., primary, Schmitt, Clemens A., primary, Schulte, Johannes H., primary, Eggert, Angelika, primary, Haase, Kerstin, primary, Kirwan, Jennifer, primary, Hagemann, Anja I.H., primary, Mertins, Philipp, primary, Dörr, Jan R., primary, and Henssen, Anton G., primary

Published
2024
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19. Figure 5 from Passenger Gene Coamplifications Create Collateral Therapeutic Vulnerabilities in Cancer

Author

Bei, Yi, primary, Bramé, Luca, primary, Kirchner, Marieluise, primary, Fritsche-Guenther, Raphaela, primary, Kunz, Severine, primary, Bhattacharya, Animesh, primary, Rusu, Mara-Camelia, primary, Gürgen, Dennis, primary, Dubios, Frank P.B., primary, Köppke, Julia K.C., primary, Proba, Jutta, primary, Wittstruck, Nadine, primary, Sidorova, Olga Alexandra, primary, Chamorro González, Rocío, primary, Dorado Garcia, Heathcliff, primary, Brückner, Lotte, primary, Xu, Robin, primary, Giurgiu, Mădălina, primary, Rodriguez-Fos, Elias, primary, Yu, Qinghao, primary, Spanjaard, Bastiaan, primary, Koche, Richard P., primary, Schmitt, Clemens A., primary, Schulte, Johannes H., primary, Eggert, Angelika, primary, Haase, Kerstin, primary, Kirwan, Jennifer, primary, Hagemann, Anja I.H., primary, Mertins, Philipp, primary, Dörr, Jan R., primary, and Henssen, Anton G., primary

Published
2024
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20. Figure 3 from Passenger Gene Coamplifications Create Collateral Therapeutic Vulnerabilities in Cancer

Author

Bei, Yi, primary, Bramé, Luca, primary, Kirchner, Marieluise, primary, Fritsche-Guenther, Raphaela, primary, Kunz, Severine, primary, Bhattacharya, Animesh, primary, Rusu, Mara-Camelia, primary, Gürgen, Dennis, primary, Dubios, Frank P.B., primary, Köppke, Julia K.C., primary, Proba, Jutta, primary, Wittstruck, Nadine, primary, Sidorova, Olga Alexandra, primary, Chamorro González, Rocío, primary, Dorado Garcia, Heathcliff, primary, Brückner, Lotte, primary, Xu, Robin, primary, Giurgiu, Mădălina, primary, Rodriguez-Fos, Elias, primary, Yu, Qinghao, primary, Spanjaard, Bastiaan, primary, Koche, Richard P., primary, Schmitt, Clemens A., primary, Schulte, Johannes H., primary, Eggert, Angelika, primary, Haase, Kerstin, primary, Kirwan, Jennifer, primary, Hagemann, Anja I.H., primary, Mertins, Philipp, primary, Dörr, Jan R., primary, and Henssen, Anton G., primary

Published
2024
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21. Figure 1 from Passenger Gene Coamplifications Create Collateral Therapeutic Vulnerabilities in Cancer

Author

Bei, Yi, primary, Bramé, Luca, primary, Kirchner, Marieluise, primary, Fritsche-Guenther, Raphaela, primary, Kunz, Severine, primary, Bhattacharya, Animesh, primary, Rusu, Mara-Camelia, primary, Gürgen, Dennis, primary, Dubios, Frank P.B., primary, Köppke, Julia K.C., primary, Proba, Jutta, primary, Wittstruck, Nadine, primary, Sidorova, Olga Alexandra, primary, Chamorro González, Rocío, primary, Dorado Garcia, Heathcliff, primary, Brückner, Lotte, primary, Xu, Robin, primary, Giurgiu, Mădălina, primary, Rodriguez-Fos, Elias, primary, Yu, Qinghao, primary, Spanjaard, Bastiaan, primary, Koche, Richard P., primary, Schmitt, Clemens A., primary, Schulte, Johannes H., primary, Eggert, Angelika, primary, Haase, Kerstin, primary, Kirwan, Jennifer, primary, Hagemann, Anja I.H., primary, Mertins, Philipp, primary, Dörr, Jan R., primary, and Henssen, Anton G., primary

Published
2024
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22. Figure 2 from Passenger Gene Coamplifications Create Collateral Therapeutic Vulnerabilities in Cancer

Author

Bei, Yi, primary, Bramé, Luca, primary, Kirchner, Marieluise, primary, Fritsche-Guenther, Raphaela, primary, Kunz, Severine, primary, Bhattacharya, Animesh, primary, Rusu, Mara-Camelia, primary, Gürgen, Dennis, primary, Dubios, Frank P.B., primary, Köppke, Julia K.C., primary, Proba, Jutta, primary, Wittstruck, Nadine, primary, Sidorova, Olga Alexandra, primary, Chamorro González, Rocío, primary, Dorado Garcia, Heathcliff, primary, Brückner, Lotte, primary, Xu, Robin, primary, Giurgiu, Mădălina, primary, Rodriguez-Fos, Elias, primary, Yu, Qinghao, primary, Spanjaard, Bastiaan, primary, Koche, Richard P., primary, Schmitt, Clemens A., primary, Schulte, Johannes H., primary, Eggert, Angelika, primary, Haase, Kerstin, primary, Kirwan, Jennifer, primary, Hagemann, Anja I.H., primary, Mertins, Philipp, primary, Dörr, Jan R., primary, and Henssen, Anton G., primary

Published
2024
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23. Protective [alpha]1-antitrypsin effects in autoimmune vasculitis are compromised by methionine oxidation

Author

Ebert, Maximilian, Jerke, Uwe, Eulenberg-Gustavus, Claudia, Kling, Lovis, Jenne, Dieter, Kirchner, Marieluise, Mertins, Philipp, Bieringer, Markus, Elitok, Saban, Eckardt, Kai-Uwe, Schreiber, Adrian, Salama, Alan D., and Kettritz, Ralph

Subjects
Vasculitis -- Development and progression -- Care and treatment, Methionine -- Health aspects -- Physiological aspects, Alpha 1-antitrypsin -- Health aspects -- Physiological aspects, Autoimmune diseases -- Development and progression -- Care and treatment, Oxidation-reduction reaction -- Health aspects -- Physiological aspects, Health care industry
Abstract

BACKGROUND. Antineutrophil cytoplasmic autoantibody-associated (ANCA-associated) vasculitidies (AAV) are lifethreatening systemic autoimmune conditions. ANCAs directed against proteinase 3 (PR3) or myeloperoxidase (MPO) bind their cell surface-presented antigen, activate neutrophils, and cause vasculitis. An imbalance between PR3 and its major inhibitor [alpha]1-antitrypsin (AAT) was proposed to underlie PR3- but not MPO-AAV. We measured AAT and PR3 in healthy individuals and patients with AAV and studied protective AAT effects pertaining to PR3- and MPO-ANCA. METHODS. Plasma and blood neutrophils were assessed for PR3 and AAT. WT, mutant, and oxidation-resistant AAT species were produced to characterize AAT-PR3 interactions by flow cytometry, immunoblotting, fluorescence resonance energy transfer assays, and surface plasmon resonance measurements. Neutrophil activation was measured using the ferricytochrome C assay and AAT methionine-oxidation by Parallel Reaction Monitoring. RESULTS. We found significantly increased PR3 and AAT pools in patients with both PR3- and MPO-AAV; however, only in PR3-AAV did the PR3 pool correlate with the ANCA titer, inflammatory response, and disease severity. Mechanistically, AAT prevented PR3 from binding to CD177, thereby reducing neutrophil surface antigen for ligation by PR3-ANCA. Active patients with PR3-AAV showed critical methionine-oxidation in plasma AAT that was recapitulated by ANCA-activated neutrophils. The protective PR3-related AAT effects were compromised by methionine-oxidation in the AAT reactive center loop but preserved when 2 critical methionines were substituted with valine and leucine. CONCLUSION. Pathogenic differences between PR3- and MPO-AAV are related to AAT regulation of membrane-PR3, attenuating neutrophil activation by PR3-ANCA rather than MPO-ANCA. Oxidation-resistant AAT could serve as adjunctive therapy in PR3-AAV. FUNDING. This work was supported by KE 576/10-1 from the Deutsche Forschungsgemeinschaft, SCHR 771/8-1 from the Deutsche Forschungsgemeinschaft, grant 394046635--SFB 1365 from the Deutsche Forschungsgemeinschaft, and ECRC grants., Introduction Antineutrophil cytoplasmic autoantibody-associated (ANCA-associated) vasculitis (AAV) comprises a group of life-threatening, systemic autoimmune diseases, most frequently affecting the lungs and kidneys (1). The majority of patients with the clinical [...]

Published
2022
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24. High serum prevalence of autoreactive IgG antibodies against peripheral nerve structures in patients with neurological post-COVID-19 vaccination syndrome.

Author

Arlt, Friederike A., Breuer, Ameli, Trampenau, Elli, Boesl, Fabian, Kirchner, Marieluise, Mertins, Philipp, Sánchez-Sendín, Elisa, Nasouti, Mahoor, Mayrhofer, Marie, Blüthner, Martin, Endres, Matthias, Prüss, Harald, and Franke, Christiana

Subjects
PERIPHERAL nervous system, NERVOUS system, MEDICAL practice, SCIATIC nerve, CELL nuclei
Abstract

Background: Patients suffering from neurological symptoms after COVID-19 vaccination (post-COVID-19 vaccination syndrome (PCVS)) have imposed an increasing challenge on medical practice, as diagnostic precision and therapeutic options are lacking. Underlying autoimmune dysfunctions, including autoantibodies, have been discussed in neurological disorders after SARSCoV-2 infection and vaccination. Here, we describe the frequency and targets of autoantibodies against peripheral nervous system tissues in PCVS. Methods: Sera from50 PCVS patients with peripheral neurological symptoms after COVID-19 vaccination and 35 vaccinated healthy controls were used in this study. IgG autoreactivity was measured via indirect immunofluorescence assays on mouse sciatic nerve teased fibers. The frequencies of autoantibodies were compared between groups using Fisher's exact test. Serum anti-ganglioside antibodies were measured in ganglioside blots. Autoantibody target identification was performed using immunoprecipitation coupled to mass spectrometry. Subsequent target confirmation was conducted via cell-based assays and ELISA. Results: Compared with controls, PCVS patients had a significantly greater frequency of autoantibodies against peripheral nervous system structures (9/50 (18%) vs 1/35(3%); p=0.04). Autoantibodies bound to paranodes (n=5), axons (n=4), Schmidt-Lanterman incisures (n=2) and Schwann cell nuclei (n=1). Conversely, antibodies against gangliosides were absent in PCVS patients. Target identification and subsequent confirmation revealed various subunits of neurofilaments as well as DFS-70 as autoantibody epitopes. Conclusion: Our data suggest that autoantibodies against nervous system tissue could be relevant in PCVS patients. Autoantibodies against neurofilaments and cell nuclei with so far non-established links to this disease spectrum should be further elucidated to determine their biomarker potential. [ABSTRACT FROM AUTHOR]

Published
2024
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25. Immunosuppression with cyclosporine versus tacrolimus shows distinctive nephrotoxicity profiles within renal compartments.

Author

Demirci, Hasan, Popovic, Suncica, Dittmayer, Carsten, Yilmaz, Duygu Elif, El‐Shimy, Ismail Amr, Mülleder, Michael, Hinze, Christian, Su, Mingzhen, Mertins, Philipp, Kirchner, Marieluise, Osmanodja, Bilgin, Paliege, Alexander, Budde, Klemens, Amann, Kerstin, Persson, Pontus B., Mutig, Kerim, and Bachmann, Sebastian

Subjects
TACROLIMUS, CYCLOSPORINE, NEPHROTOXICOLOGY, TRANSPLANTATION of organs, tissues, etc., IMMUNOSUPPRESSION, RENAL tubular transport disorders
Abstract

Aim: Calcineurin inhibitors (CNIs) are the backbone for immunosuppression after solid organ transplantation. Although successful in preventing kidney transplant rejection, their nephrotoxic side effects contribute to allograft injury. Renal parenchymal lesions occur for cyclosporine A (CsA) as well as for the currently favored tacrolimus (Tac). We aimed to study whether chronic CsA and Tac exposures, before reaching irreversible nephrotoxic damage, affect renal compartments differentially and whether related pathogenic mechanisms can be identified. Methods: CsA and Tac were administered chronically in wild type Wistar rats using osmotic minipumps over 4 weeks. Functional parameters were controlled. Electron microscopy, confocal, and 3D‐structured illumination microscopy were used for histopathology. Clinical translatability was tested in human renal biopsies. Standard biochemical, RNA‐seq, and proteomic technologies were applied to identify implicated molecular pathways. Results: Both drugs caused significant albeit differential damage in vasculature and nephron. The glomerular filtration barrier was more affected by Tac than by CsA, showing prominent deteriorations in endothelium and podocytes along with impaired VEGF/VEGFR2 signaling and podocyte‐specific gene expression. By contrast, proximal tubule epithelia were more severely affected by CsA than by Tac, revealing lysosomal dysfunction, enhanced apoptosis, impaired proteostasis and oxidative stress. Lesion characteristics were confirmed in human renal biopsies. Conclusion: We conclude that pathogenetic alterations in the renal compartments are specific for either treatment. Considering translation to the clinical setting, CNI choice should reflect individual risk factors for renal vasculature and tubular epithelia. As a step in this direction, we share protein signatures identified from multiomics with potential pathognomonic relevance. [ABSTRACT FROM AUTHOR]

Published
2024
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26. Herpes simplex virus type 1 modifies the protein composition of extracellular vesicles to promote neurite outgrowth and neuroinfection

Author

Sun, Guorong, primary, Kropp, Kai Alexander, additional, Kirchner, Marieluise, additional, Plückebaum, Nina, additional, Selich, Anton, additional, Serrero, Manutea, additional, Dhingra, Akshay, additional, Cabrera, Jorge Rubén, additional, Ritter, Birgit, additional, Bauerfeind, Rudolf, additional, Wyler, Emanuel, additional, Landthaler, Markus, additional, Schambach, Axel, additional, Sodeik, Beate, additional, Mertins, Philipp, additional, and Viejo-Borbolla, Abel, additional

Published
2024
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27. Passenger gene co-amplifications create collateral therapeutic vulnerabilities in cancer

Author

Bei, Yi, primary, Brame, Luca, additional, Kirchner, Marieluise, additional, Fritsche-Guenther, Raphaela, additional, Kunz, Severine, additional, Bhattacharya, Animesh, additional, Rusu, Mara-Camelia, additional, Gurgen, Dennis, additional, Dubois, Frank P.B., additional, Koppke, Julia K.C., additional, Proba, Jutta, additional, Wittstruck, Nadine, additional, Sidorova, Olga Alexandra., additional, Chamorro Gonzalez, Rocío, additional, Dorado Garcia, Heathcliff, additional, Bruckner, Lotte, additional, Xu, Robin, additional, Giurgiu, Madalina, additional, Rodriguez-Fos, Elias, additional, Yu, Qinghao, additional, Spanjaard, Bastiaan, additional, Koche, Richard P., additional, Schmitt, Clemens A., additional, Schulte, Johannes H., additional, Eggert, Angelika, additional, Haase, Kerstin, additional, Kirwan, Jennifer, additional, Hagemann, Anja IH., additional, Mertins, Philipp, additional, Dorr, Jan R., additional, and Henssen, Anton G., additional

Published
2024
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32. Aberrant N-glycosylation in pathogenic variants of adenosine deaminase 2 underlying human ADA2 deficiency

Author

Ehlers, Lisa, primary, Hombrouck, Anneleen, additional, Wouters, Marjon, additional, Pillay, Bethany, additional, Delafontaine, Selket, additional, Bucciol, Giorgia, additional, Baggio, Marco, additional, Dzhus, Mariia, additional, Jacquemyn, Maarten, additional, De Somer, Lien, additional, Schrijvers, Rik, additional, Vanderschueren, Steven, additional, Cassiman, David, additional, Kirchner, Marieluise, additional, Mertins, Philipp, additional, Kallinich, Tilmann, additional, Daelemans, Dirk, additional, Agostinis, Patrizia, additional, Moens, Leen, additional, and Meyts, Isabelle, additional

Published
2023
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33. Prdm16 mutation determines sex-specific cardiac metabolism and identifies two novel cardiac metabolic regulators

Author

Kühnisch, Jirko, primary, Theisen, Simon, additional, Dartsch, Josephine, additional, Fritsche-Guenther, Raphaela, additional, Kirchner, Marieluise, additional, Obermayer, Benedikt, additional, Bauer, Anna, additional, Kahlert, Anne-Karin, additional, Rothe, Michael, additional, Beule, Dieter, additional, Heuser, Arnd, additional, Mertins, Philipp, additional, Kirwan, Jennifer A, additional, Berndt, Nikolaus, additional, MacRae, Calum A, additional, Hubner, Norbert, additional, and Klaassen, Sabine, additional

Published
2023
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34. Proteomic analysis reveals upregulation of ACE2, the putative SARS-CoV-2 receptor in pressure- but not volume-overloaded human hearts

Author

Stegbauer, Johannes, Kraus, Milena, Nordmeyer, Sarah, Kirchner, Marieluise, Ziehm, Matthias, Dommisch, Henrik, Kelle, Sebastian, Kelm, Marcus, Baczkó, István, Landmesser, Ulf, Tschöpe, Carsten, Knosalla, Christoph, Falcke, Martin, Schapranow, Matthieu-P., Regitz-Zagrosek, Vera, Mertins, Philipp, and Kuehne, Titus

Published
2020
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37. CLCN2 chloride channel mutations in familial hyperaldosteronism type II

Author

Scholl, Ute I., Stölting, Gabriel, Schewe, Julia, Thiel, Anne, Tan, Hua, Nelson-Williams, Carol, Vichot, Alfred A., Jin, Sheng Chih, Loring, Erin, Untiet, Verena, Yoo, Taekyeong, Choi, Jungmin, Xu, Shengxin, Wu, Aihua, Kirchner, Marieluise, Mertins, Philipp, Rump, Lars C., Onder, Ali Mirza, Gamble, Cory, McKenney, Daniel, Lash, Robert W., Jones, Deborah P., Chune, Gary, Gagliardi, Priscila, Choi, Murim, Gordon, Richard, Stowasser, Michael, Fahlke, Christoph, and Lifton, Richard P.

Published
2018
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38. Effects of Elexacaftor/Tezacaftor/Ivacaftor on Sputum Viscoelastic Properties, Airway Infection and Inflammation in Patients with Cystic Fibrosis

Author

Graeber, Simon, additional, Addante, Annalisa, additional, Völler, MIrjam, additional, Schaupp, Laura, additional, Fentker, Kerstin, additional, Bardua, Markus, additional, Kuppe, Aditi, additional, Duerr, Julia, additional, Piehler, Linus, additional, Röhmel, Jobst, additional, Thee, Stephanie, additional, Kirchner, Marieluise, additional, Ziehm, Matthias, additional, Lauster, Daniel, additional, Haag, Rainer, additional, Gradzielski, Michael, additional, Stahl, Mirjam, additional, Mertins, Philipp, additional, Boutin, Sebastien, additional, and Mall, MarcusA., additional

Published
2023
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40. A proteomics analysis of 5xFAD mouse brain regions reveals the lysosome-associated protein Arl8b as a candidate biomarker for Alzheimer’s disease

Author

Boeddrich, Annett, primary, Haenig, Christian, additional, Neuendorf, Nancy, additional, Blanc, Eric, additional, Ivanov, Andranik, additional, Kirchner, Marieluise, additional, Schleumann, Philipp, additional, Bayraktaroğlu, Irem, additional, Richter, Matthias, additional, Molenda, Christine Mirjam, additional, Sporbert, Anje, additional, Zenkner, Martina, additional, Schnoegl, Sigrid, additional, Suenkel, Christin, additional, Schneider, Luisa-Sophie, additional, Rybak-Wolf, Agnieszka, additional, Kochnowsky, Bianca, additional, Byrne, Lauren M., additional, Wild, Edward J., additional, Nielsen, Jørgen E., additional, Dittmar, Gunnar, additional, Peters, Oliver, additional, Beule, Dieter, additional, and Wanker, Erich E., additional

Published
2023
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41. Disease- and sex-specific differences in patients with heart valve disease: a proteome study

Author

Nordmeyer, Sarah, primary, Kraus, Milena, additional, Ziehm, Matthias, additional, Kirchner, Marieluise, additional, Schafstedde, Marie, additional, Kelm, Marcus, additional, Niquet, Sylvia, additional, Stephen, Mariet Mathew, additional, Baczko, Istvan, additional, Knosalla, Christoph, additional, Schapranow, Matthieu-P, additional, Dittmar, Gunnar, additional, Gotthardt, Michael, additional, Falcke, Martin, additional, Regitz-Zagrosek, Vera, additional, Kuehne, Titus, additional, and Mertins, Philipp, additional

Published
2023
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42. Prdm16mutation determines sex-specific cardiac metabolism and identifies two novel cardiac metabolic regulators

Author

Kühnisch, Jirko, primary, Theisen, Simon, additional, Dartsch, Josephine, additional, Fritsche-Guenther, Raphaela, additional, Kirchner, Marieluise, additional, Obermayer, Benedikt, additional, Bauer, Anna, additional, Kahlert, Anne-Karin, additional, Rothe, Michael, additional, Beule, Dieter, additional, Heuser, Arnd, additional, Mertins, Philipp, additional, Kirwan, Jennifer A., additional, Berndt, Nikolaus, additional, MacRae, Calum A., additional, Hubner, Norbert, additional, and Klaassen, Sabine, additional

Published
2023
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43. Effects of Elexacaftor/Tezacaftor/Ivacaftor on Sputum Viscoelastic Properties, Airway Infection and Inflammation in Patients with Cystic Fibrosis

Author

Addante, Annalisa, primary, Völler, Mirjam, additional, Schaupp, Laura, additional, Fentker, Kerstin, additional, Bardua, Markus, additional, Kuppe, Aditi, additional, Duerr, Julia, additional, Piehler, Linus, additional, Röhmel, Jobst, additional, Thee, Stephanie, additional, Kirchner, Marieluise, additional, Ziehm, Matthias, additional, Lauster, Daniel, additional, Haag, Rainer, additional, Gradzielski, Michael, additional, Stahl, Mirjam, additional, Mertins, Philipp, additional, Boutin, Sébastien, additional, Graeber, Simon Y., additional, and Mall, Marcus A., additional

Published
2022
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44. Protective α1-antitrypsin effects in autoimmune vasculitis are compromised by methionine oxidation

Author

Ebert, Maximilian, primary, Jerke, Uwe, additional, Eulenberg-Gustavus, Claudia, additional, Kling, Lovis, additional, Jenne, Dieter, additional, Kirchner, Marieluise, additional, Mertins, Philipp, additional, Bieringer, Markus, additional, Elitok, Saban, additional, Eckardt, Kai-Uwe, additional, Schreiber, Adrian, additional, Salama, Alan D., additional, and Kettritz, Ralph, additional

Published
2022
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45. Additional file 1 of A proteomics analysis of 5xFAD mouse brain regions reveals the lysosome-associated protein Arl8b as a candidate biomarker for Alzheimer’s disease

Author

Boeddrich, Annett, Haenig, Christian, Neuendorf, Nancy, Blanc, Eric, Ivanov, Andranik, Kirchner, Marieluise, Schleumann, Philipp, Bayraktaroğlu, Irem, Richter, Matthias, Molenda, Christine Mirjam, Sporbert, Anje, Zenkner, Martina, Schnoegl, Sigrid, Suenkel, Christin, Schneider, Luisa-Sophie, Rybak-Wolf, Agnieszka, Kochnowsky, Bianca, Byrne, Lauren M., Wild, Edward J., Nielsen, Jørgen E., Dittmar, Gunnar, Peters, Oliver, Beule, Dieter, and Wanker, Erich E.

Abstract

Additional file 1: Table S1. Commercial antibodies used in this study. Table S2. Characteristics of AD and HD patients and corresponding controls. Table S3. Spearman correlation analysis of Arl8b protein level measurements and AD biomarker levels.

Published
2023
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46. Additional file 2 of A proteomics analysis of 5xFAD mouse brain regions reveals the lysosome-associated protein Arl8b as a candidate biomarker for Alzheimer’s disease

Author

Boeddrich, Annett, Haenig, Christian, Neuendorf, Nancy, Blanc, Eric, Ivanov, Andranik, Kirchner, Marieluise, Schleumann, Philipp, Bayraktaroğlu, Irem, Richter, Matthias, Molenda, Christine Mirjam, Sporbert, Anje, Zenkner, Martina, Schnoegl, Sigrid, Suenkel, Christin, Schneider, Luisa-Sophie, Rybak-Wolf, Agnieszka, Kochnowsky, Bianca, Byrne, Lauren M., Wild, Edward J., Nielsen, Jørgen E., Dittmar, Gunnar, Peters, Oliver, Beule, Dieter, and Wanker, Erich E.

Abstract

Additional file 2: Fig. S1. Aβ peptide levels and APP and PSEN1 expression in hippocampus and cortex of 5xFAD mice. Fig. S2. Analysis of Aβ aggregate formation using membrane filter assays and sucrose gradient centrifugations. Fig. S3. Analysis of wild-type expression profiles to assess whether the protein abundance changes detected in 5xFAD brains are more frequent among highly expressed mouse proteins. Fig. S4. Functional analysis of dysregulated proteins defined with a pairwise model in brains of 5xFAD mice. Fig. S5. Enrichment analysis of cell-type-specific marker proteins among dysregulated proteins in brains of 5xFAD mice. Fig. S6. IPA and gene ontology enrichment analysis of differentially expressed proteins defined with the full model in cortical and hippocampal tissues of 5xFAD mice. Fig. S7. Ingenuity pathway analysis of Aβ-correlated and anticorrelated DEPs defined by the pairwise model in brains of 5xFAD mice. Fig. S8. Numbers of pairwise common DEPs in the mouse datasets and datasets from human studies. Fig. S9. Strategy to define mouse protein signatures that are concordantly altered also in AD patient brains. Fig. S10. Investigation of the overlap of DEPs in brains of 5xFAD mice with DEPs in asymptomatic AD brains. Fig. S11. Analysis of the correlation in protein effect sizes between 5xFAD mouse and AD patient brains for proteins present in all studies. Fig. S12. Selection of the neuronal lysosome-associated protein Arl8b by step-by-step data filtering. Fig. S13. Immunofluorescence analysis of 5xFAD brain slices. Fig. S14. Analysis of Arl8b protein aggregates using human brain homogenates derived from AD patients and control individuals.

Published
2023
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47. Amplicon structure creates collateral therapeutic vulnerability in cancer

Author

Bei, Yi, primary, Bramé, Luca, additional, Kirchner, Marieluise, additional, Fritsche-Guenther, Raphaela, additional, Kunz, Sevrine, additional, Bhattacharya, Animesh, additional, Köppke, Julia, additional, Proba, Jutta, additional, Wittstruck, Nadine, additional, Sidorova, Olga A., additional, González, Rocío Chamorro, additional, Garcia, Heathcliff Dorado, additional, Brückner, Lotte, additional, Xu, Robin, additional, Giurgiu, Mădălina, additional, Rodriguez-Fos, Elias, additional, Koche, Richard, additional, Schmitt, Clemens, additional, Schulte, Johannes H., additional, Eggert, Angelika, additional, Haase, Kerstin, additional, Kirwan, Jennifer, additional, Hagemann, Anja I.H., additional, Mertins, Philipp, additional, Dörr, Jan R., additional, and Henssen, Anton G., additional

Published
2022
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48. Defining the landscape of circular RNAs in neuroblastoma unveils a global suppressive function of MYCN.

Author

Fuchs, Steffen, Danßmann, Clara, Klironomos, Filippos, Winkler, Annika, Fallmann, Jörg, Kruetzfeldt, Louisa-Marie, Szymansky, Annabell, Naderi, Julian, Bernhart, Stephan H., Grunewald, Laura, Helmsauer, Konstantin, Rodriguez-Fos, Elias, Kirchner, Marieluise, Mertins, Philipp, Astrahantseff, Kathy, Suenkel, Christin, Toedling, Joern, Meggetto, Fabienne, Remke, Marc, and Stadler, Peter F.

Subjects
CIRCULAR RNA, NEUROBLASTOMA, GENE expression, RNA helicase, CHILDHOOD cancer, RNA-binding proteins, TUMOR suppressor genes
Abstract

Circular RNAs (circRNAs) are a regulatory RNA class. While cancer-driving functions have been identified for single circRNAs, how they modulate gene expression in cancer is not well understood. We investigate circRNA expression in the pediatric malignancy, neuroblastoma, through deep whole-transcriptome sequencing in 104 primary neuroblastomas covering all risk groups. We demonstrate that MYCN amplification, which defines a subset of high-risk cases, causes globally suppressed circRNA biogenesis directly dependent on the DHX9 RNA helicase. We detect similar mechanisms in shaping circRNA expression in the pediatric cancer medulloblastoma implying a general MYCN effect. Comparisons to other cancers identify 25 circRNAs that are specifically upregulated in neuroblastoma, including circARID1A. Transcribed from the ARID1A tumor suppressor gene, circARID1A promotes cell growth and survival, mediated by direct interaction with the KHSRP RNA-binding protein. Our study highlights the importance of MYCN regulating circRNAs in cancer and identifies molecular mechanisms, which explain their contribution to neuroblastoma pathogenesis. The role of circular RNAs (circRNAs) in modulating gene expression in cancer remains to be investigated. Here, the authors perform whole transcriptome sequencing in 104 primary neuroblastomas and reveal the involvement of MYCN in regulating circRNAs. [ABSTRACT FROM AUTHOR]

Published
2023
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49. Frequent ZNF217mutations lead to transcriptional deregulation of interferon signal transduction via altered chromatin accessibility in B cell lymphoma

Author

Briest, Franziska, Noerenberg, Daniel, Hennch, Cornelius, Yoshida, Kenichi, Hablesreiter, Raphael, Nimo, Jose, Sasca, Daniel, Kirchner, Marieluise, Mansouri, Larry, Inoue, Yoshikage, Wiegand, Laura, Staiger, Annette M., Casadei, Beatrice, Korkolopoulou, Penelope, Weiner, January, Lopez-Guillermo, Armando, Warth, Arne, Schneider, Tamás, Nagy, Ákos, Klapper, Wolfram, Hummel, Michael, Kanellis, George, Anagnostopoulos, Ioannis, Mertins, Philipp, Bullinger, Lars, Rosenquist, Richard, Vassilakopoulos, Theodoros P., Ott, German, Ogawa, Seishi, and Damm, Frederik

Abstract

Recent exome-wide studies discovered frequent somatic mutations in the epigenetic modifier ZNF217in primary mediastinal B cell lymphoma (PMBCL) and related disorders. As functional consequences of ZNF217alterations remain unknown, we comprehensively evaluated their impact in PMBCL. Targeted sequencing identified genetic lesions affecting ZNF217in 33% of 157 PMBCL patients. Subsequent gene expression profiling (n= 120) revealed changes in cytokine and interferon signal transduction in ZNF217-aberrant PMBCL cases. In vitro, knockout of ZNF217led to changes in chromatin accessibility interfering with binding motifs for crucial lymphoma-associated transcription factors. This led to disturbed expression of interferon-responsive and inflammation-associated genes, altered cell behavior, and aberrant differentiation. Mass spectrometry demonstrates that ZNF217 acts within a histone modifier complex containing LSD1, CoREST and HDAC and interferes with H3K4 methylation and H3K27 acetylation. Concluding, our data suggest non-catalytic activity of ZNF217, which directs histone modifier complex function and controls B cell differentiation-associated patterns of chromatin structure.

Published
2023
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50. Pyruvate dehydrogenase kinases as a potential novel target to treat osteoarthritis

Author

Damerau, Alexandra, additional, Kirchner, Marieluise, additional, Pfeiffenberger, Moritz, additional, Ehlers, Lisa, additional, Do, Ha Nguyen Duc, additional, Mertins, Philipp, additional, Bartek, Benjamin, additional, Maleitzke, Tazio, additional, Palmowski, Yannick, additional, Hardt, Sebastian, additional, Winkler, Tobias, additional, Buttgereit, Frank, additional, and Gaber, Timo, additional

Published
2022
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