A5072342706- Herpesvirus Infections and Treatments
- Dermatology and Skin Diseases
- Skin and Cellular Biology Research
- Poxvirus research and outbreaks
- Microtubule and mitosis dynamics
- Cytomegalovirus and herpesvirus research
- Biochemical and Molecular Research
- Contact Dermatitis and Allergies
- Trypanosoma species research and implications
- Food Allergy and Anaphylaxis Research
- Wnt/β-catenin signaling in development and cancer
- Research on Leishmaniasis Studies
- Transgenic Plants and Applications
- RNA regulation and disease
- Hair Growth and Disorders
- Immune Cell Function and Interaction
- Reproductive Biology and Fertility
- Cancer-related gene regulation
- Cancer and Skin Lesions
- Allergic Rhinitis and Sensitization
- Neurological diseases and metabolism
- Plant Reproductive Biology
- Chemical Synthesis and Analysis
- Cutaneous Melanoma Detection and Management
- Toxin Mechanisms and Immunotoxins
University of Cologne
2019-2025
Cologne Excellence Cluster on Cellular Stress Responses in Aging Associated Diseases
2020-2025
University Hospital Cologne
2019-2022
Heidelberg University
1996
Abstract The development of complex stratified epithelial barriers in mammals is initiated from single-layered epithelia. How stratification and fueled are still open questions. Previous studies on skin epidermal suggested a central role for perpendicular/asymmetric cell division orientation the basal keratinocyte progenitors. Here, we use centrosomes, that organize mitotic spindle, to test whether linked. Genetically ablating centrosomes developing epidermis leads activation p53-, 53BP1-...
African trypanosomes are extracellular protozoan parasites that transmitted from one mammalian host to the next by tsetse flies. Bloodstream forms express variant surface glycoprotein (VSG); fly (procyclic) instead procyclic acidic repetitive protein (PARP). PARP mRNA is abundant in and almost undetectable blood-stream forms. Post-transcriptional mechanisms mainly responsible for regulation but results of nuclear run-on experiments suggested transcription might also be regulated. We measured...
Ectodermal appendage formation requires hedgehog (HH) signal reception, its conduction through the primary cilium and activation of Gli transcription factors (TF). How HH signalling induces cell-type-specific responses TF in stem cells (SCs) their ciliadependence remain open questions. Here, we use conditional mouse mutants to genetically dissect roles cilia mediators skin epithelium. Upon Gli2 depletion, hair follicle (HF) morphogenesis is delayed whereas sebaceous gland (SG) enhanced,...
To infect its human host, herpes simplex virus 1 (HSV-1) must overcome the protective barriers of skin and mucosa. Here, we addressed whether pathological conditions can facilitate viral entry via surface used ex vivo infection studies to explore invasion in atopic dermatitis (AD) characterized by disturbed barrier functions. Our focus was on visualization onset single cells determine primary portals epidermis. After lesional AD skin, observed infected suprabasal layers indicating successful...
Herpes simplex virus 1 (HSV-1) enters its human host via the skin and mucosa. The open question is how invades this highly protective tissue in vivo to approach receptors epidermis initiate infection. Here, we performed ex infection studies investigate susceptible dermis are HSV-1 whether wounding facilitates viral invasion. Upon of complete skin, only sample edges with integrity loss demonstrated infected cells. After removal dermis, efficiently invaded basal layer and, from there, gained...
Skin is a major target tissue of herpes simplex virus 1 (HSV-1), and we are only beginning to understand how individual receptors contribute the initiation infection in tissue. We recently demonstrated impact nectin-1 herpesvirus entry mediator (HVEM) for HSV-1 into murine epidermis. Here, focus on viral invasion dermis, further critical vivo In principle, dermal fibroblasts highly susceptible HSV-1, previously showed that HVEM can act as alternative receptors. To characterize their...
Dynamin GTPases, best known for their role in membrane fission of endocytic vesicles, provide a target viruses to be exploited during uptake. Recently, we found that entry herpes simplex virus 1 (HSV-1) into skin cells depends on dynamin, although our results supported viral internalization occurs via both direct fusion with the plasma and pathways. To further explore dynamin efficient HSV-1 entry, utilized conditional 2 double-knockout (DKO) fibroblasts as an experimental tool. Strikingly,...
Although herpes simplex virus 1 (HSV-1) is a well-studied virus, how the invades its human host via skin and mucosa to reach receptors initiate infection remains an open question. For studies of HSV-1 in skin, mice have been used as animal models. Murine can be induced after injection or scratching which provides insights into disease pathogenesis but clearly distinct from natural entry route tissue. To explore invasion on tissue level, we established ex vivo assay using explants. Here,...
Abstract The development of complex stratified epithelial barriers in mammals is initiated from single-layered epithelia. How stratification and fueled are still open questions. Previous studies on skin epidermal suggested a central role for perpendicular/asymmetric cell division orientation the basal keratinocyte progenitors. Here, we use centrosomes, that organize mitotic spindle, to test whether linked. Genetically ablating centrosomes developing epidermis led activation p53-, 53BP1-...
Abstract Herpes simplex virus 1 (HSV-1) enters its human host via the skin or mucosa. The open question is how invades this highly protective tissue in vivo to approach receptors epidermis and initiate infection. Here, we performed ex infection studies investigate susceptible dermis are HSV-1 whether wounding facilitates viral invasion. Upon of complete skin, only sample edges demonstrated infected cells. After removal dermis, efficiently invaded basal layer, from there, gained access...
Herpes simplex virus 1 (HSV-1) invades its human host via the skin and mucosa initiates infection in epithelium. While murine epidermis are highly susceptible to HSV-1, we recently observed rare infected cells dermis only minor efficiency upon ex vivo infection. Here, investigated why so inefficiently explored potential differences between dermal fibroblasts. In principle, primary fibroblasts HSV-1; however, found a delayed onset compared cells. Intriguingly, of was evident collagen-embedded...