Thomas Sommermann

Max Delbrück Center

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Ellen Cahir-McFarland

Annexon Biosciences (United States)

David R. Plas

University of Cincinnati Medical Center

Kathleen O’Neill

University of Pennsylvania

Klaus Rajewsky

Harvard University

Van Trung Chu

Max Delbrück Center

Timm Weber

Max Delbrück Center

Robin Graf

Max Delbrück Center

Ralf Kühn

Max Delbrück Center

Tomoharu Yasuda

Hiroshima University

Kerstin Petsch

Max Delbrück Center

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Technical University of Munich

Max Delbrück Center

German Cancer Research Center

Harvard University

Deutschen Konsortium für Translationale Krebsforschung

Heidelberg University

Charité - Universitätsmedizin Berlin

Brigham and Women's Hospital

Molecular Oncology (United States)

Freie Universität Berlin

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Supplementary Figure 4 from IKKβ and NF-κB Transcription Govern Lymphoma Cell Survival through AKT-Induced Plasma Membrane Trafficking of GLUT1

Thomas Sommermann Kathleen O’Neill David R. Plas Ellen Cahir-McFarland

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10.1158/0008-5472.22390407

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Supplementary Figure 2 from IKKβ and NF-κB Transcription Govern Lymphoma Cell Survival through AKT-Induced Plasma Membrane Trafficking of GLUT1

Thomas Sommermann Kathleen O’Neill David R. Plas Ellen Cahir-McFarland

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10.1158/0008-5472.22390413

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Efficient CRISPR/Cas9-Mediated Gene Knockin in Mouse Hematopoietic Stem and Progenitor Cells

Cell Reports (2019)

Ngoc Tung Tran Thomas Sommermann Robin Graf Janine Trombke Jenniffer Pempe

Mutations accumulating in hematopoietic stem and progenitor cells (HSPCs) during development can cause severe hematological disorders. Modeling these mutations in mice is essential for understanding their functional consequences. Here, we describe an efficient CRISPR/Cas9-based system to knock in and repair genes in mouse HSPCs. CRISPR/Cas9 ribonucleoproteins, in combination with recombinant adeno-associated virus (rAAV)-DJ donor templates, led to gene knockin efficiencies of up to 30% in the Lmnb1 and Actb loci of mouse HSPCs in vitro. The targeted HSPCs engraft and reconstitute all immune cell lineages in the recipient mice. Using this approach, we corrected a neomycin-disrupted Rag2 gene. The Rag2-corrected HSPCs restore B and T cell development in vivo, confirming the functionality of the approach. Our method provides an efficient strategy to study gene function in the hematopoietic system and model hematological disorders in vivo, without the need for germline mutagenesis.

10.1016/j.celrep.2019.08.065

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Supplementary Figure 3 from IKKβ and NF-κB Transcription Govern Lymphoma Cell Survival through AKT-Induced Plasma Membrane Trafficking of GLUT1

Thomas Sommermann Kathleen O’Neill David R. Plas Ellen Cahir-McFarland

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10.1158/0008-5472.22390410

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Supplementary Figure 1A-G from IKKβ and NF-κB Transcription Govern Lymphoma Cell Survival through AKT-Induced Plasma Membrane Trafficking of GLUT1

Thomas Sommermann Kathleen O’Neill David R. Plas Ellen Cahir-McFarland

PDF file - 524K

10.1158/0008-5472.22390419.v1

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Supplementary Figure 2 from IKKβ and NF-κB Transcription Govern Lymphoma Cell Survival through AKT-Induced Plasma Membrane Trafficking of GLUT1

Thomas Sommermann Kathleen O’Neill David R. Plas Ellen Cahir-McFarland

PDF file - 478K

10.1158/0008-5472.22390413.v1

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Data from IKKβ and NF-κB Transcription Govern Lymphoma Cell Survival through AKT-Induced Plasma Membrane Trafficking of GLUT1

Thomas Sommermann Kathleen O’Neill David R. Plas Ellen Cahir-McFarland

<div>AbstractAll cancer cells require increased nutrient uptake to support proliferation. In this study, we investigated the signals that govern glucose uptake in B-cell lymphomas and determined that the inhibitor of NF-κB-kinase β (IKKβ) induced glucose transporter-1 (GLUT1) membrane trafficking in both viral and spontaneous B-cell lymphomas. IKKβ induced AKT activity, whereas IKKβ-driven NF-κB transcription was required for GLUT1 surface localization downstream of AKT. Activated NF-κB promoted AKT-mediated phosphorylation of the GLUT1 regulator, AKT substrate of 160kD (AS160), but was not required for AKT phosphorylation of the mTOR regulator Tuberous Sclerosis 2 (TSC2). In Epstein-Barr virus–transformed B cells, NF-κB inhibition repressed glucose uptake and induced caspase-independent cell death associated with autophagy. After NF-κB inhibition, an alternate carbon source ameliorated both autophagy and cell death, whereas autophagy inhibitors specifically accelerated cell death. Taken together, the results indicate that NF-κB signaling establishes a metabolic program supporting proliferation and apoptosis resistance by driving glucose import. Cancer Res; 71(23); 7291–300. ©2011 AACR.</div>

IκB kinase

IκBα

10.1158/0008-5472.c.6502938.v1

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LMP1 and EBNA2 constitute a minimal set of EBV genes for transformation of human B cells

Frontiers in Immunology (2023)

Jingwei Zhang Thomas Sommermann Xun Li Lutz Gieselmann Kathrin de la Rosa

Introduction Epstein-Barr virus (EBV) infection in humans is associated with a wide range of diseases including malignancies of different origins, most prominently B cells. Several EBV latent genes are thought to act together in B cell immortalization, but a minimal set of EBV genes sufficient for transformation remains to be identified. Methods Here, we addressed this question by transducing human peripheral B cells from EBV-negative donors with retrovirus expressing the latent EBV genes encoding Latent Membrane Protein (LMP) 1 and 2A and Epstein-Barr Nuclear Antigen (EBNA) 2. Results LMP1 together with EBNA2, but not LMP1 alone or in combination with LMP2A was able to transform human primary B cells. LMP1/EBNA2-immortalized cell lines shared surface markers with EBV-transformed lymphoblastoid cell lines (LCLs). They showed sustained growth for more than 60 days, albeit at a lower growth rate than EBV-transformed LCLs. LMP1/EBNA2-immortalized cell lines generated tumors when transplanted subcutaneously into severely immunodeficient NOG mice. Conclusion Our results identify a minimal set of EBV proteins sufficient for B cell transformation.

Immortalised cell line

10.3389/fimmu.2023.1331730

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Supplementary Figure 1A-G from IKKβ and NF-κB Transcription Govern Lymphoma Cell Survival through AKT-Induced Plasma Membrane Trafficking of GLUT1

Thomas Sommermann Kathleen O’Neill David R. Plas Ellen Cahir-McFarland

PDF file - 524K

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10.1158/0008-5472.22390419

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Data from IKKβ and NF-κB Transcription Govern Lymphoma Cell Survival through AKT-Induced Plasma Membrane Trafficking of GLUT1