A5024126273- Pancreatic function and diabetes
- Metabolism, Diabetes, and Cancer
- Endoplasmic Reticulum Stress and Disease
- Animal Genetics and Reproduction
- Genomics and Chromatin Dynamics
- Enzyme Structure and Function
- Diabetes and associated disorders
- Biochemical and Molecular Research
- Cancer therapeutics and mechanisms
- Pancreatic and Hepatic Oncology Research
- Viral gastroenteritis research and epidemiology
- Animal health and immunology
- Epigenetics and DNA Methylation
- Cellular transport and secretion
- Hippo pathway signaling and YAP/TAZ
- DNA Repair Mechanisms
- Porphyrin Metabolism and Disorders
- RNA Research and Splicing
- RNA modifications and cancer
- Clostridium difficile and Clostridium perfringens research
- Autophagy in Disease and Therapy
- Milk Quality and Mastitis in Dairy Cows
- Viral Infectious Diseases and Gene Expression in Insects
- Cancer-related Molecular Pathways
- Pancreatitis Pathology and Treatment
Deutsches Diabetes-Zentrum e.V.
2018-2023
Heinrich Heine University Düsseldorf
2018-2023
German Center for Diabetes Research
2018-2023
University Medical Center of the Johannes Gutenberg University Mainz
2021
Johannes Gutenberg University Mainz
2021
Technical University of Munich
2017-2018
University of Zurich
2008
ETH Zurich
2007
Universität Hamburg
2003
Vitamin B1 (thiamin) is an essential compound in all organisms acting as a cofactor key metabolic reactions and has furthermore been implicated responses to DNA damage pathogen attack plants. Despite the fact that it was discovered almost century ago deficiency widespread health problem, much remains be deciphered about its biosynthesis. The vitamin composed of thiazole pyrimidine heterocycle, which can synthesized by prokaryotes, fungi, Plants are major source human diet, yet little known...
Impaired proinsulin-to-insulin processing in pancreatic β-cells is a key defective step both type 1 diabetes and 2 (T2D) (refs.
Abstract Myc proteins are essential regulators of cellular growth and proliferation during normal development. Activating mutations in myc genes result excessive frequently associated with human cancers. At the same time, forced expression sensitizes vertebrate cells towards different pro‐apoptotic stimuli. Recently, ability overexpressed to induce cell‐autonomous apoptosis has been shown be evolutionarily conserved Drosophila (dMyc). Here, we show that dMyc induced is accompanied by...
Beta cell dysfunction and death are critical steps in the development of both type 1 2 diabetes (T1D T2D), but underlying mechanisms incompletely understood. Activation essential tumor suppressor transcription factor P53 (also known as TP53 Trp53 mice) was linked to beta vitro has been reported several mouse models cells humans with T2D. In this article, we set out determine specific role dysfunction, vivo.We generated knockout (P53BKO) mice used complementary genetic, dietary...
Differential cloning revealed a partial mRNA sequence expressed in the mouse testis, which on further molecular characterization proved to be member of new family 14 transcribed genes. Six genes appear pseudogenes. The remainder indicate an open reading frame approximately 200–220 amino acids encoding proteins with very high proportion alpha helical secondary structure, comprising 15% glutamate residues. Because this property, has been named SPErm-associated (E)-Rich protein (SPEER). Three...
Pancreatic beta cell death is a hallmark of type 1 and 2 diabetes (T1D/T2D), but the underlying molecular mechanisms are incompletely understood. Key proteins DNA damage response (DDR), including tumor protein P53 (P53, also known as TP53 or TRP53 in rodents) Ataxia Telangiectasia Mutated (ATM), kinase to act upstream P53, have been associated with T2D. Here we test compare effect ATM ablation on survival rat line Ins1E. We demonstrate that differentially regulate apoptosis induced upon...
The oxidation-induced DNA modification 8-oxo-7,8-dihydro-2′-deoxyguanosine (8-oxodG) was recently implicated in the activation and repression of gene transcription. We aimed at a systematic characterisation impacts 8-oxodG on activity GC box placed upstream from RNA polymerase II core promoter. With help reporters carrying single synthetic residues four conserved G:C base pairs (underlined) within 5′-TGGGCGGAGC-3′ sequence, we identified two modes interference with promoter activity....
Stepwise oxidation of the epigenetic mark 5-methylcytosine and base excision repair (BER) resulting 5-formylcytosine (5-fC) 5-carboxycytosine (5-caC) may provide a mechanism for reactivation epigenetically silenced genes; however, functions 5-fC 5-caC at defined gene elements are scarcely explored. We analyzed expression reporter constructs containing either 2'-deoxy-(5-fC/5-caC) or their BER-resistant 2'-fluorinated analogs, asymmetrically incorporated into CG-dinucleotide GC box...
New treatment options are needed to prevent relapses following failed antibiotic therapies of Clostridium difficile infections (CDI) in humans. The concomitant therapy with an anti-C. IgA containing whey protein concentrate can support the sustainable recovery CDI patients. For 31 weeks, nine dairy cows were continuously vaccinated several vaccines by certain routes administration produce enriched milk. study aimed at finding decisive differences between low responder (LR) and high (HR) (>...
Background Beta cell dysfunction and death are critical steps in the development of both type 1 2 diabetes (T1D T2D), but underlying mechanisms incompletely understood. Activation essential tumor suppressor transcription factor P53 was linked to beta vitro has been reported several mouse models cells humans with T2D. Therefore, we investigated specific role dysfunction, vivo.
One of the pathomechanisms linked to development Type 2 Diabetes is reduction pancreatic beta cell mass due apoptosis. Although canonical tumor suppressor Tp53 a critical regulator death, its specific function in cells remains unclear. We aimed determine impact and associated network on survival cell.
The reduction of pancreatic beta cell mass due to apoptosis has been linked type 2 diabetes etiology. tumor suppressor Tp53 is a critical regulator death and may regulate survival in the context diabetes. We investigated molecular pathways modulated by vitro impact specific ablation models vivo.
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