F. Thomas Wunderlich

ORCID: 0000-0002-9209-3501
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About
Contact & Profiles
Research Areas
  • Malaria Research and Control
  • Immune Cell Function and Interaction
  • Adipose Tissue and Metabolism
  • Adipokines, Inflammation, and Metabolic Diseases
  • Lipid Membrane Structure and Behavior
  • Regulation of Appetite and Obesity
  • Cancer-related gene regulation
  • CAR-T cell therapy research
  • T-cell and B-cell Immunology
  • HER2/EGFR in Cancer Research
  • Coccidia and coccidiosis research
  • Mosquito-borne diseases and control
  • RNA Research and Splicing
  • Lymphoma Diagnosis and Treatment
  • Protist diversity and phylogeny
  • Cytokine Signaling Pathways and Interactions
  • RNA modifications and cancer
  • Trypanosoma species research and implications
  • Research on Leishmaniasis Studies
  • Methane Hydrates and Related Phenomena
  • Hormonal and reproductive studies
  • Monoclonal and Polyclonal Antibodies Research
  • RNA Interference and Gene Delivery
  • Helminth infection and control
  • Vector-borne infectious diseases

Max Planck Institute for Metabolism Research
2016-2025

Cologne Excellence Cluster on Cellular Stress Responses in Aging Associated Diseases
2016-2025

University of Cologne
2015-2025

Heinrich Heine University Düsseldorf
2013-2025

University Hospital Cologne
2009-2025

Max Planck Society
1972-2015

Institute of Genetics
2005-2013

King Saud University
2010-2013

Max Planck Institute for Biology of Ageing
2009

Friedrich Schiller University Jena
2001-2007

Prohibitins comprise an evolutionarily conserved and ubiquitously expressed family of membrane proteins with poorly described functions. Large assemblies PHB1 PHB2 subunits are localized in the inner mitochondria, but various roles other cellular compartments have also been proposed for both proteins. Here, we used conditional gene targeting murine Phb2 to define activities prohibitins. Our experiments restrict function prohibitins mitochondria identify processing dynamin-like GTPase OPA1,...

10.1101/gad.460708 article EN Genes & Development 2008-02-15

Highlights•Central IL-6 action suppresses feeding and improves glucose tolerance•IL-6-mediated metabolic actions via the CNS are enhanced in obesity•Beneficial central effects on metabolism exerted trans-signaling•Blocking of trans-signaling PVH attenuates its beneficial effectsSummaryInterleukin (IL)-6 engages similar signaling mechanisms to leptin. Here, we find that application mice tolerance. In contrast leptin, whose is attenuated obesity, ability suppress obese mice. absence neuronal...

10.1016/j.celrep.2017.03.043 article EN cc-by-nc-nd Cell Reports 2017-04-01

Sensory neurons relay gut-derived signals to the brain, yet molecular and functional organization of distinct populations remains unclear. Here, we employed intersectional genetic manipulations probe feeding glucoregulatory function sensory neurons. We reconstruct gut innervation patterns numerous molecularly defined vagal spinal afferents identify their downstream brain targets. Bidirectional chemogenetic manipulations, coupled with behavioral circuit mapping analysis, demonstrated that...

10.1016/j.cmet.2021.05.002 article EN cc-by Cell Metabolism 2021-05-26

Abstract Pro-opiomelanocortin (POMC)-expressing neurons in the arcuate nucleus of hypothalamus represent key regulators metabolic homeostasis. Electrophysiological and single-cell sequencing experiments have revealed a remarkable degree heterogeneity these neurons. However, exact molecular basis functional consequences this not yet been addressed. Here, we developed new mouse models which intersectional Cre/Dre-dependent recombination allowed for successful labeling, translational profiling...

10.1038/s41593-021-00854-0 article EN cc-by Nature Neuroscience 2021-05-17

T cells are considered to be unresponsive testosterone due the absence of androgen receptors (AR). Here, we demonstrate responsiveness murine splenic in vitro as well presence unconventional cell surface for and classical intracellular AR. Binding sites on both CD4+ CD8+ subsets directly revealed with impeded ligand testosterone-BSA-FITC by confocal laser scanning microscopy (CLSM) flow cytometry, respectively. plasma membrane impermeable testosterone-BSA conjugate induces a rapid rise (<5s)...

10.1096/fasebj.13.1.123 article EN The FASEB Journal 1999-01-01

Insulin resistance is a hallmark of type 2 diabetes, and many insights into the functions insulin have been gained through study mice lacking IR. To gain better understanding role action in brain versus peripheral tissues, we created mouse models with inducible IR inactivation, 1 all tissues including (IRDeltawb), restricted to (IRDeltaper). While downregulation expression resulted severe hyperinsulinemia both models, hyperglycemia was more pronounced IRDeltawb mice. Both strains displayed...

10.1172/jci31073 article EN Journal of Clinical Investigation 2008-04-30

Testosterone acts on cells through intracellular transcription-regulating androgen receptors (ARs). Here, we show that mouse IC-21 macrophages lack the classical AR yet exhibit specific nongenomic responses to testosterone. These manifest themselves as testosterone-induced rapid increase in free [Ca(2+)], which is due release of Ca(2+) from stores. This mobilization also inducible by plasma membrane-impermeable testosterone-BSA. It not affected blockers cyproterone and flutamide, whereas it...

10.1091/mbc.10.10.3113 article EN Molecular Biology of the Cell 1999-10-01

Leptin-stimulated Stat3 activation in proopiomelanocortin (POMC)-expressing neurons of the hypothalamus plays an important role maintenance energy homeostasis. While POMC is required for expression, elevated basal as present development obesity has not been directly addressed. Here, we have generated and characterized mice expressing a constitutively active version (Stat3-C) (Stat3-C mice). On normal chow diet, these animals develop result hyperphagia decreased expression accompanied by...

10.1523/jneurosci.5712-08.2009 article EN cc-by-nc-sa Journal of Neuroscience 2009-09-16

Abstract Colorectal cancer (CRC) is one of the most lethal cancers worldwide in which vast majority cases exhibit little genetic risk but are associated with a sedentary lifestyle and obesity. Although mechanisms underlying CRC colitis-associated colorectal (CAC) remain unclear, we hypothesised that obesity-induced inflammation predisposes to CAC development. Here, show diet-induced obesity accelerates chemically-induced mice via increased immune cell recruitment. Obesity-induced...

10.1038/s41467-018-03773-0 article EN cc-by Nature Communications 2018-04-19

c-Jun N-terminal kinase (JNK) 1-dependent signaling plays a crucial role in the development of obesity-associated insulin resistance. Here we demonstrate that JNK activation not only occurs peripheral tissues, but also hypothalamus and pituitary obese mice. To resolve importance JNK1 hypothalamic/pituitary circuitry, have generated mice with conditional inactivation nestin-expressing cells (JNK1 ΔNES mice). exhibit improved sensitivity both CNS glucose metabolism, as well protection from...

10.1073/pnas.1001796107 article EN Proceedings of the National Academy of Sciences 2010-03-15
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