A5039760583- Adipose Tissue and Metabolism
- Pancreatic function and diabetes
- Epigenetics and DNA Methylation
- Neuroinflammation and Neurodegeneration Mechanisms
- Diabetes Treatment and Management
- RNA modifications and cancer
- Peptidase Inhibition and Analysis
- Diet and metabolism studies
- Diabetes and associated disorders
- Neuropeptides and Animal Physiology
- Genomics and Chromatin Dynamics
- Neurological Disease Mechanisms and Treatments
- Regulation of Appetite and Obesity
- Chromosomal and Genetic Variations
- Adipokines, Inflammation, and Metabolic Diseases
- Genetic Associations and Epidemiology
- CRISPR and Genetic Engineering
- Immune cells in cancer
- Parkinson's Disease Mechanisms and Treatments
- Neurobiology and Insect Physiology Research
- Hedgehog Signaling Pathway Studies
- Nutrition, Genetics, and Disease
- Receptor Mechanisms and Signaling
- Maternal Mental Health During Pregnancy and Postpartum
- Birth, Development, and Health
Max Planck Institute of Immunobiology and Epigenetics
2015-2025
Van Andel Institute
2018-2025
Max Planck Society
2010-2015
Focus (Germany)
2011
Austrian Academy of Sciences
2006-2010
Institute of Molecular Biotechnology
2006-2010
University of British Columbia
2000-2004
Activation of the innate immune system in obesity is a risk factor for development type 2 diabetes. The aim current study was to investigate notion that increased numbers macrophages exist islets diabetes patients and this may be explained by dysregulation islet-derived inflammatory factors. Increased islet-associated cells were observed human diabetic patients, high-fat–fed C57BL/6J mice, GK rat, db/db mouse. When cultured exposed milieu or when isolated from factors produced released,...
Innate Immunity in the Fly Gut Drosophila melanogaster is an important model system to study innate immunity, being both easy manipulate and lacking adaptive immune system. In order identify genes that regulate Cronin et al. (p. 340 ; published online 11 June) performed RNA interference screen on flies infected with oral bacterial pathogen, Serratia marcescens . Genes involved intestinal immunity regulation of hemocytes, macrophage-like cells critical for phagocytosis killing bacteria, were...
Epigenetic modifications on DNA and histones regulate gene expression by modulating chromatin accessibility to transcription machinery. Here we identify methionine as a key nutrient affecting epigenetic reprogramming in CD4+ T helper (Th) cells. Using metabolomics, showed that is rapidly taken up activated cells serves the major substrate for biosynthesis of universal methyl donor S-adenosyl-L-methionine (SAM). Methionine was required maintain intracellular SAM pools restriction reduced...
The gut microbiome can impact brain health and is altered in Parkinson’s disease (PD). vermiform appendix a lymphoid tissue the cecum implicated storage regulation of microbiota. We sought to determine whether PD analyze biological consequences microbial alterations. investigated changes functional microbiota patients relative controls (n = 12 PD, 16 C) by metatranscriptomic analysis. found dysbiosis affecting lipid metabolism, including an upregulation bacteria responsible for secondary...
We have developed a mouse DNA methylation array that contains 296,070 probes representing the diversity of biology. present atlas as rich reference resource 1,239 samples encompassing distinct tissues, strains, ages, sexes, and pathologies. describe applications for comparative epigenomics, genomic imprinting, epigenetic inhibitors, patient-derived xenograft assessment, backcross tracing, clocks. dissect processes associated with differentiation, aging, tumorigenesis. Notably, we find...
The gut microbiome and its metabolites can impact brain health are altered in Parkinson's disease (PD) patients. It has been recently demonstrated that PD patients have reduced fecal levels of the potent epigenetic modulator butyrate bacterial producers.Here, we investigate whether changes associated related to symptoms markers leucocytes neurons.Stool, whole blood samples, clinical data were collected from 55 controls. We performed DNA methylation analysis on samples analyzed results...
Recent studies into the physiology of incretins glucose-dependent insulinotropic polypeptide (GIP) and glucagon-like peptide-1 (GLP-1) have added stimulation β-cell growth, differentiation, cell survival to well-documented, potent effects. Unfortunately, therapeutic potential these hormones is limited by their rapid enzymatic inactivation in vivo dipeptidyl peptidase IV (DP IV). Inhibition DP IV, so as enhance circulating incretin levels, has proved effective treatment type 2 diabetes both...
The incretins, glucose-dependent insulinotropic polypeptide (GIP) and glucagon-like peptide 1 (GLP-1) are responsible for >50% of nutrient-stimulated insulin secretion. After being released into the circulation, GIP GLP-1 rapidly inactivated by circulating enzyme dipeptidyl peptidase IV (DP IV). use DP inhibitors to enhance these hormonal axes has proven effective on an acute scale in both animals humans; however, long-term effects compounds have yet be determined. Therefore, we...
To date, it remains largely unclear to what extent chromatin machinery contributes the susceptibility and progression of complex diseases. Here, we combine deep epigenome mapping with single-cell transcriptomics mine for evidence dysregulation in type 2 diabetes. We find two chromatin-state signatures that track β cell dysfunction mice humans: ectopic activation bivalent Polycomb-silenced domains loss expression at an epigenomically unique class lineage-defining genes. cell-specific Polycomb...
The mechanisms that specify and stabilize cell subtypes remain poorly understood. Here, we identify two major of pancreatic β cells based on histone mark heterogeneity (β
The incretin glucose-dependent insulinotropic polypeptide (GIP) is a major regulator of postprandial insulin secretion in mammals. Recent studies our laboratory, and others have suggested that GIP potent stimulus for protein kinase activation, including the MAPK (ERK1/2) module. Based on these studies, we hypothesized could regulate cell fate sought to examine underlying mechanisms involved stimulation survival. potentiated glucose-induced beta-(INS-1)-cell growth levels comparable with GH...