A5001339980- Cell death mechanisms and regulation
- Autophagy in Disease and Therapy
- Metabolism and Genetic Disorders
- Phagocytosis and Immune Regulation
- Cardiac Arrhythmias and Treatments
- Adrenal Hormones and Disorders
- RNA Interference and Gene Delivery
- Erythrocyte Function and Pathophysiology
- Cancer-related Molecular Pathways
- Mitochondrial Function and Pathology
- Microbial Natural Products and Biosynthesis
- Liver Disease Diagnosis and Treatment
- Adenosine and Purinergic Signaling
- Biochemical and Molecular Research
- Liver Diseases and Immunity
- Signaling Pathways in Disease
- Dermatological and Skeletal Disorders
- Immune Cell Function and Interaction
- Connective tissue disorders research
- Aortic Disease and Treatment Approaches
- Lysosomal Storage Disorders Research
- Diabetes and associated disorders
- Cell Adhesion Molecules Research
- Peptidase Inhibition and Analysis
- NF-κB Signaling Pathways
Düsseldorf University Hospital
2012-2025
Heinrich Heine University Düsseldorf
2016-2025
Institute of Molecular Medicine
2013-2022
Faculty (United Kingdom)
2017-2020
Hochschule Düsseldorf University of Applied Sciences
2017
University of Tübingen
2004-2013
University Children's Hospital Tübingen
2008
Justus-Liebig-Universität Gießen
2007
University Gastroenterology
2006
Universitätsklinikum Tübingen
2005-2006
Abstract The complex formed by two members of the S100 calcium-binding protein family, S100A8/A9, exerts apoptosis-inducing activity against various cells, especially tumor cells. Here, we present evidence that S100A8/A9 also has cell growth-promoting at low concentrations. Receptor advanced glycation end product (RAGE) gene silencing and cotreatment with a RAGE-specific blocking antibody revealed this was mediated via RAGE ligation. To investigate signaling pathways, MAPK phosphorylation...
Unc-51-like kinase 1 (Ulk1) plays a central role in autophagy induction. It forms stable complex with Atg13 and focal adhesion (FAK) family interacting protein of 200 kDa (FIP 200). This is negatively regulated by the mammalian target rapamycin (mTORC1) nutrient-dependent way. AMP-activated (AMPK), which activated LKB1/Strad/Mo25 upon high AMP levels, stimulates inhibiting mTORC1. Recently, it has been described that AMPK Ulk1 interact latter phosphorylated AMPK. phosphorylation leads to...
Abstract Ferroptosis is a form of regulated cell death that emerges to be relevant for therapy-resistant and dedifferentiating cancers. Although several lines evidence suggest ferroptosis type autophagy-dependent death, the underlying molecular mechanisms remain unclear. Fin56, 3 inducer, triggers by promoting glutathione peroxidase 4 (GPX4) protein degradation via not fully understood pathway. Here, we determined Fin56 induces autophagy in bladder cancer cells Fin56-triggered...
Signaling via the CD3/TCR complex induces programmed cell death (apoptosis) in immature thymocytes and transformed T lymphocytes (hybridomas or leukemic cells). Accumulating evidence indicates, however, that apoptosis can be triggered also mature peripheral cells. Here we show a significant fraction of cells given IL-2-dependent TCR-alpha beta + clone polyclonal short term line is killed when cultured for 20 h presence PHA, anti-CD3 (OKT3), anti-TCR (BMA031) mAb. Apoptosis by these stimuli...
Cells of the macrophage lineage express a peculiar surface receptor for extracellular ATP, designated P2Z/P2X7 purinergic receptor, that induces pore formation and collapse plasma membrane potential. Although function P2Z is largely unknown, accumulating evidence implicates its role in cell signaling immune reactions. Here, we investigated effect ligation on activation NF-κB, transcription factor controlling cytokine expression apoptosis. Exposure microglial cells to ATP but not other...
Myeloic cells express a peculiar surface receptor for extracellular ATP, called the P2Z/P2X 7 purinoreceptor, which is involved in cell death signalling. Here, we investigated role of caspases, family proteases implicated apoptosis and cytokine secretion. We observed that ATP induced activation multiple caspases including caspase‐1, ‐3 ‐8, subsequent cleavage caspase substrates PARP lamin B. Using inhibitors, it was found were specifically ATP‐induced apoptotic damage such as chromatin...
Mitogen-activated protein (MAP) kinases are important mediators of the cellular stress response. Here, we investigated relationship between activation MAP kinase p38 and transcription factor NF-κB. Different forms were found to preferentially trigger either or Arsenite osmotic potently activated but ineffective in inducing NF-κB activation. Tumor necrosis factor-α hydrogen peroxide, contrast, led only modestly stimulated p38. The was strongly abolished by antioxidants, while activity AP-1...
Phagocytosis of apoptotic cells is fundamentally important throughout life, because non-cleared become secondarily necrotic and release intracellular contents, thus instigating inflammatory autoimmune responses. Secreted "find-me" exposed "eat-me" signals displayed by the dying cell in concert with phagocyte receptors comprise phagocytic synapse clearance. In this scenario, lysophospholipids (lysoPLs) are assumed to act as find-me for attraction phagocytes. However, both identity lyso-PLs...
Apoptosis is induced by different stimuli, among them triggering of the death receptor CD95, staurosporine, and chemotherapeutic drugs. In all cases, apoptosis mediated caspases, although it unclear how these diverse apoptotic stimuli cause protease activation. Two regulatory pathways have been recently identified, but remains unknown whether they are functionally independent or linked to each other. One recruitment proximal regulator caspase-8 complex. The other pathway controlled release...
Activation-induced cell death of T lymphocytes requires the inducible expression CD95 (APO-1/Fas) ligand, which triggers apoptosis in CD95-bearing target cells by an autocrine or paracrine mechanism. Although execution pathway is largely independent reactive oxygen intermediates, activation-induced blocked a variety antioxidants. In present study, we investigated involvement redox processes regulation ligand (CD95L) Jurkat cells. We show that various antioxidants potently inhibited...
Here, we show that CDK2, an S-phase cyclin-dependent kinase, is a novel target for Akt during cell cycle progression and apoptosis. phosphorylates CDK2 at threonine 39 residue both in vitro vivo. Although phosphorylation mediated by enhances cyclin-A binding, it dispensable its basal binding the kinase activity. In addition, first time, report transient nucleo-cytoplasmic shuttling of specific stages cycle, particular late S G2 phases. The re-localized to nucleus causes temporary cytoplasmic...