A5102710721- NF-κB Signaling Pathways
- Immune Response and Inflammation
- FOXO transcription factor regulation
- Immune Cell Function and Interaction
- T-cell and B-cell Immunology
- Lymphoma Diagnosis and Treatment
- Neuroinflammation and Neurodegeneration Mechanisms
- Cytokine Signaling Pathways and Interactions
- RNA regulation and disease
- Pancreatitis Pathology and Treatment
- Cancer Cells and Metastasis
- Viral-associated cancers and disorders
- Pancreatic and Hepatic Oncology Research
- Cancer-related molecular mechanisms research
- Signaling Pathways in Disease
- Liver Disease Diagnosis and Treatment
- Cell death mechanisms and regulation
- Natural product bioactivities and synthesis
- TGF-β signaling in diseases
- interferon and immune responses
- Pancreatic function and diabetes
- Shoulder Injury and Treatment
- Epigenetics and DNA Methylation
- Alcohol Consumption and Health Effects
- Immunotherapy and Immune Responses
Medizinische Hochschule Hannover
2012-2025
Universität Ulm
2015-2024
Olgahospital
2017-2020
University Hospital Ulm
2019
Klinikum Stuttgart
2017-2018
University of Eastern Finland
2008-2012
Physiological Society
2012
University of Tübingen
2009
University of Bern
2009
Seibersdorf Laboratories (Austria)
2005
The transcription factor NF-κB is activated in a range of human cancers and thought to promote tumorigenesis, mainly due its ability protect transformed cells from apoptosis. To investigate the role epithelial plasticity metastasis, we utilized well-characterized vitro/in vivo model mammary carcinogenesis that depends on collaboration Ha-Ras oncoprotein TGF-β. We show here IKK-2/IκBα/NF-κB pathway required for induction maintenance epithelial-mesenchymal transition (EMT). Inhibition...
The transcription factor NF-κB is activated in a range of human cancers and thought to promote tumorigenesis, mainly due its ability protect transformed cells from apoptosis. To investigate the role epithelial plasticity metastasis, we utilized well-characterized vitro/in vivo model mammary carcinogenesis that depends on collaboration Ha-Ras oncoprotein TGF-β. We show here IKK-2/IκBα/NF-κB pathway required for induction maintenance epithelial-mesenchymal transition (EMT). Inhibition...
In this study we have identified members of the Toll-like receptor (TLR) family (namely, TLRs 4, 6, 8, and 9) as proteins to which intracellular protein tyrosine kinase, Bruton's kinase (Btk), binds. Detailed analysis interaction between Btk TLR8 demonstrates that presence both Box 2 3 motifs in Toll/interleukin-1 domain was required for interaction. Furthermore, co-immunoprecipitation experiments revealed can also interact with key involved TLR4 signal transduction, namely, MyD88, Mal...
Activation of the transcription factor NF-κB is necessary for full expression tumor necrosis α (TNF-α)-inducible endothelial chemokines and adhesion molecules. However, a detailed analysis regarding contribution different upstream components to activation has not been performed yet. We employed retroviral infection approach stably express transdominant (TD) mutants IκBα, IκBβ, or IκBε dominant negative (dn) versions IκB kinases (IKK) 1 2 as well constitutively active version IKK2 in human...
Inflammation is a major factor in heart disease. IκB kinase (IKK) and its downstream target NF-κB are regulators of inflammation activated cardiac disorders, but their precise contributions targets unclear. We analyzed IKK/NF-κB function the by gain-of-function approach, generating an inducible transgenic mouse model with cardiomyocyte-specific expression constitutively active IKK2. In adult animals, IKK2 activation led to inflammatory dilated cardiomyopathy failure. Transgenic hearts showed...
Article6 June 2018Open Access Source DataTransparent process NF-κB activation in astrocytes drives a stage-specific beneficial neuroimmunological response ALS Najwa Ouali Alami Department of Neurology, Ulm University, Ulm, Germany Search for more papers by this author Christine Schurr Institute Physiological Chemistry, Florian Olde Heuvel Linyun Tang Qian Li orcid.org/0000-0002-6621-2167 Alpaslan Tasdogan Immunology, Atsushi Kimbara Roche Pharma Research and Early Development, Innovation...
Alterations of learning and memory in mice with deregulated neuron-specific nuclear factor κB (NF-κB) activity support the idea that plastic changes synaptic contacts may depend at least part on IκB kinase (IKK)/NF-κB-related synapse-to-nucleus signaling. There is, however, little information molecular requirements mechanisms regulating this IKK/NF-κB-dependent synapse development remodeling. Here, we report NF-κB inducing IKK complex is localized postsynaptic density (PSD) activated under...
Liver damage in humans is induced by various insults including alcohol abuse, hepatitis B/C virus infection, autoimmune or metabolic disorders and, when persistent, leads to development of liver fibrosis. Because the nuclear factor-κB (NF-κB) system activated response several these stresses, we hypothesized that NF-κB activation hepatocytes may contribute fibrosis development. To activate signaling pathway a time- and cell-type-specific manner liver, crossed transgenic mice carrying...
NF-κB is essential for effective transcription of primate lentiviral genomes and also activates antiviral host genes. Here, we show that the early protein Nef most lentiviruses enhances activation. In contrast, late Vpu HIV-1 its simian precursors inhibits activation NF-κB, even in presence Nef. Although this effect did not correlate with ability to interact β-TrCP, it involved stabilization IκB reduced nuclear translocation p65. Interestingly, however, affect casein kinase II-mediated...
Inflammaging represents an accepted concept where the immune system shifts to a low-grade chronic pro-inflammatory state without overt infection upon aging. In CNS, inflammaging is mainly driven by glia cells and associated with neurodegenerative processes. White matter degeneration (WMD), well-known process in aging brain, manifests myelin loss finally resulting motor, sensory cognitive impairments. Oligodendrocytes (OL) are responsible for homeostasis maintenance of sheaths, which complex...
NF-κB is regulated by inhibitor proteins (IκBs), which retain in the cytoplasm. Signal-induced phosphorylation IκB-kinase complex containing IκB-kinases 1 and 2 (IKK-1/2 or IKK-α/β) subsequent degradation of IκB are prerequisites for activation. Many signals induce NF-κB, one them being oncogenic Raf kinase. We investigated whether induction critical Raf-mediated transformation. Here, we demonstrate that inhibition interferes with transformation Raf-oncogene, characterized mechanism...
AbstractActivation of the transcription factor NF-?B occurs in many human tumors, and studies have shown that NF-κB can promote cell proliferation oncogenesis, possibly by protecting cells from apoptosis. Little is known, however, about whether involved tumor progression including epithelial-mesenchymal transition (EMT), a central process governing both morphogenesis carcinoma multicellular organisms. In combined vitro/in vivo model mammary carcinogenesis, was essential for induction...
Transforming growth factor beta (TGF-beta) has a growth-inhibitory effect on numerous different cell types of the immune system, including T lymphocytes. We show in this study that inhibitory action TGF-beta lymphocytes is accompanied by block interleukin 2 (IL-2) gene expression which mediated, at least part, inhibition IL-2 promoter/enhancer activity. The functional analysis cis-regulatory (proto-enhancer) elements enhancer/promoter region showed most TGF-beta-responsive element maps to...