A5088291740- Cancer-related Molecular Pathways
- Lipid metabolism and disorders
- Peroxisome Proliferator-Activated Receptors
- Cholesterol and Lipid Metabolism
- Nuclear Receptors and Signaling
- Ubiquitin and proteasome pathways
- Acute Myeloid Leukemia Research
- Diabetes, Cardiovascular Risks, and Lipoproteins
- Lymphoma Diagnosis and Treatment
- Metabolism, Diabetes, and Cancer
- Drug Transport and Resistance Mechanisms
- Olfactory and Sensory Function Studies
- Advanced Chemical Sensor Technologies
- Chronic Myeloid Leukemia Treatments
- Sarcoma Diagnosis and Treatment
- Blood groups and transfusion
- Free Radicals and Antioxidants
- Metabolomics and Mass Spectrometry Studies
- Pancreatic function and diabetes
- Atherosclerosis and Cardiovascular Diseases
- Cancer, Lipids, and Metabolism
- Cytokine Signaling Pathways and Interactions
- Erythrocyte Function and Pathophysiology
- DNA Repair Mechanisms
- Protein Tyrosine Phosphatases
Innsbruck Medical University
2007-2024
Universität Innsbruck
2001-2024
Institut Pasteur de Lille
2005-2008
Université de Lille
2005-2008
Inserm
2004-2008
Genfit (France)
2005
Institut Pasteur
2004
The apolipoprotein A5 gene (APOA5) has been repeatedly implicated in lowering plasma triglyceride levels.Since several studies have demonstrated that hyperinsulinemia is associated with hypertriglyceridemia, we sought to determine whether APOA5 regulated by insulin.Here, show cell lines and mice treated insulin down-regulate expression a dose-dependent manner.Furthermore, found decreases human promoter activity, subsequent deletion mutation analyses uncovered functional E box the...
Alterations in the expression of recently discovered apolipoprotein A5 gene strongly affect plasma triglyceride levels. In this study, we investigated contribution APOA5 to liver X receptor (LXR) ligand-mediated effect on Following treatment with LXR ligand T0901317, found that mRNA levels were decreased hepatoma cell lines. The observation no down-regulation promoter activity was obtained by LXR-retinoid (RXR) co-transfection prompted us explore possible involvement known target SREBP-1c...
Glucocorticoid therapy is an important treatment modality of hematological malignancies, especially T-cell acute lymphoblastic leukemia (T-ALL). Glucocorticoids are known to induce a cell cycle arrest and apoptosis in T-lymphoma cells. We could demonstrate that the induced by synthetic glucocorticoid dexamethasone (Dex) clearly precedes human CEM T-ALL murine S49.1 Cyclin D3 strongly downregulated, whereas CDK inhibitor p27 (Kip1) (p27) upregulated response these RNAi-mediated knockdown as...
In addition to their role in programmed cell death, caspases exert non-lethal functions diverse developmental processes including differentiation or tissue remodeling. Terminal cycle exit and can be promoted by increased level of the CDK inhibitor p27Kip1. Activated cause proteolytic processing p27, we identified a novel caspase cleavage site human p27 that removes C-terminal fragment 22 amino acids from inhibitor, phosphodegron. Thereby, protect SCF-Skp2-mediated degradation S, G2 M phases...
P27 Kip1 (p27) can prevent cell proliferation by inactivating cyclin-dependent kinases. This function is impaired upon phosphorylation of p27 at tyrosine residue 88. We observed that FLT3 and FLT3-ITD directly bind selectively phosphorylate on this residue. Inhibition in lines strongly reduced 88 resulted increased levels cycle arrest. Subsequent analysis revealed the presence phosphorylated primary patient samples. kinase activity with AC220 significantly cells isolated from wild type...
Erythrocyte biogenesis needs to be tightly regulated secure oxygen transport and control plasma viscosity. The cytokine erythropoietin (Epo) governs erythropoiesis by promoting cell proliferation, differentiation, survival of erythroid precursor cells. Erythroid differentiation is associated with an accumulation the cyclin–dependent kinase inhibitor p27Kip1, but regulation role p27 during proliferation remain largely unknown. We observed that can bind receptor (EpoR). Activation EpoR leads...
Abstract The cyclin-dependent kinase (CDK) inhibitor p27 Kip1 regulates cell proliferation. Phosphorylation of tyrosine residue 88 (Y88) converts the into an assembly factor and activator CDKs, since Y88-phosphorylation restores activity to cyclin E,A/CDK2 enables active D/CDK4,6. To investigate physiological significance phosphorylation, we have generated a knock-in mouse model where Y88 was replaced by phenylalanine (p27-Y88F). Young p27-Y88F mice developed moderately reduced body weight,...