- Immune Cell Function and Interaction
- T-cell and B-cell Immunology
- Immunotherapy and Immune Responses
- Acute Myeloid Leukemia Research
- CRISPR and Genetic Engineering
- Protein Degradation and Inhibitors
- CAR-T cell therapy research
- IL-33, ST2, and ILC Pathways
- Acute Lymphoblastic Leukemia research
- RNA modifications and cancer
- Kruppel-like factors research
- Genomics and Chromatin Dynamics
- Complement system in diseases
- Endoplasmic Reticulum Stress and Disease
- Retinoids in leukemia and cellular processes
- Chronic Lymphocytic Leukemia Research
- T-cell and Retrovirus Studies
- Cholangiocarcinoma and Gallbladder Cancer Studies
- Cancer-related molecular mechanisms research
- Autophagy in Disease and Therapy
- Viral-associated cancers and disorders
- RNA and protein synthesis mechanisms
- PI3K/AKT/mTOR signaling in cancer
- NF-κB Signaling Pathways
- Lymphoma Diagnosis and Treatment
Research Institute of Molecular Pathology
2012-2024
Vienna Biocenter
2011-2021
Tissue-resident memory T (Trm) cells permanently localize to portals of pathogen entry, where they provide immediate protection against reinfection. To enforce tissue retention, Trm up-regulate CD69 and down-regulate molecules associated with egress; however, a Trm-specific transcriptional regulator has not been identified. Here, we show that the transcription factor Hobit is specifically up-regulated in and, together related Blimp1, mediates development skin, gut, liver, kidney mice. The...
Abstract The unfolded protein response ( UPR ) is a conserved stress‐signaling pathway activated after accumulation of proteins within the endoplasmic reticulum ER ). Active signaling leads to unconventional, enzymatic splicing XBP1 mRNA enabling expression transcription factor XBP1s control homeostasis. While IRE1 has been identified as endoribonuclease required for cleavage this mRNA, corresponding ligase in mammalian cells remained elusive. Here, we report that RTCB , catalytic subunit...
Abstract The basic helix–loop–helix (bHLH) family of transcription factors recognizes DNA motifs known as E-boxes (CANNTG) and includes 108 members 1 . Here we investigate how chromatinized are engaged by two structurally diverse bHLH proteins: the proto-oncogene MYC-MAX circadian factor CLOCK-BMAL1 (refs. 2,3 ). Both bind to preferentially near nucleosomal entry–exit sites. Structural studies with engineered or native nucleosome sequences show that triggers release from histones gain...
The transcription factor EBF1 is essential for lineage specification in early B cell development. In this study, we demonstrate by conditional mutagenesis that required commitment, pro–B development, and subsequent transition to the pre–B stage. Later was generation maintenance of several mature types. Marginal zone B-1 cells were lost, whereas follicular (FO) germinal center (GC) reduced absence EBF1. Activation receptor resulted impaired intracellular signaling, proliferation survival...
NK cells can be grouped into distinct subsets that are localized to different organs and exhibit a capacity secrete cytokines mediate cytotoxicity. Despite these hallmarks reflect tissue-specific specialization in cells, little is known about the factors control development of subsets. The basic leucine zipper transcription factor Nfil3 (E4bp4) essential for bone marrow-derived cell development, but it not clear whether equally important all or how induces lineage commitment. In this...
The transcription factor inhibitor of DNA binding (Id)2 modulates T cell fate decisions, but the molecular mechanism underpinning this regulation is unclear. In study we show that loss Id2 cripples effector differentiation and instead programs CD8(+) cells to adopt a memory with increased Eomesodermin Tcf7 expression. We demonstrate restrains by inhibiting E2A-mediated direct activation expression level mirrors recall capacity. As result defective differentiation, Id2-deficient fail induce...
Pax5 controls the generation, proliferation, and survival of all mature B cells by promoting PI3K signaling via PTEN down-regulation.
Primary liver cancer (PLC) comprises hepatocellular carcinoma (HCC) and intrahepatic cholangiocarcinoma (iCCA), two frequent lethal tumour types that differ regarding their biology responses to therapies. Liver cells harbour a high degree of cellular plasticity can give rise either HCC or iCCA. However, little is known about the cell-intrinsic mechanisms directing an oncogenically transformed cell The scope this study was identify factors determining lineage commitment in PLC.
// Stefanie Schlager 1 , Carina Salomon Sabine Olt Christoph Albrecht Anja Ebert 2 Oliver Bergner Johannes Wachter Francesca Trapani Daniel Gerlach Tilman Voss Anna Traunbauer Julian Jude Matthias Hinterndorfer Martina Minnich Norbert Schweifer Sophia M. Blake 3 Vittoria Zinzalla Barbara Drobits Darryl B. McConnell Kraut Mark Pearson Zuber 4 and Manfred Koegl Boehringer Ingelheim RCV GmbH & Co KG, Vienna, Austria Research Institute of Molecular Pathology (IMP), Vienna BioCenter (VBC),...
Article29 November 2018Open Access Transparent process Precocious expression of Blimp1 in B cells causes autoimmune disease with increased self-reactive plasma Peter Bönelt Research Institute Molecular Pathology (IMP), Vienna Biocenter (VBC), Vienna, Austria Search for more papers by this author Miriam Wöhner Martina Minnich Hiromi Tagoh Maria Fischer Markus Jaritz Anoop Kavirayani Core Facilities (VBCF), Manasa Garimella Department Microbiology, Tumor and Cell Biology, Karolinska Institute,...
During unresolved infections, some viruses escape immunological control and establish a persistant reservoir in certain cell types, such as human immunodeficiency virus (HIV), which persists follicular helper T cells (TFH cells), Epstein-Barr (EBV), B cells. Here we identified specialized group of cytotoxic (TC cells) that expressed the chemokine receptor CXCR5, selectively entered follicles eradicated infected TFH The differentiation these cells, have called 'follicular cells' (TFC required...
Background: Chromosomal rearrangements leading to overexpression of EVI1 (MECOM) on chromosome 3q26 define a distinct subtype acute myeloid leukemia (AML) that is associated with chemotherapy resistance and 2-year survival <10%. While genetic events driving aberrant expression are increasingly understood, the molecular functions drive leukemogenesis unclear, which has so far precluded development targeted therapeutics. Aims: We aimed elucidate transcriptional programs maintained by...