A5065050285- Cell Adhesion Molecules Research
- Bacterial Infections and Vaccines
- Peptidase Inhibition and Analysis
- Monoclonal and Polyclonal Antibodies Research
- Cellular Mechanics and Interactions
- Biochemical and Structural Characterization
- Radiopharmaceutical Chemistry and Applications
- Protease and Inhibitor Mechanisms
- Helicobacter pylori-related gastroenterology studies
- Coccidia and coccidiosis research
- Antimicrobial Resistance in Staphylococcus
- Escherichia coli research studies
- Ubiquitin and proteasome pathways
- Antimicrobial Peptides and Activities
- Immune Response and Inflammation
- Platelet Disorders and Treatments
- Bacterial Genetics and Biotechnology
- Reproductive tract infections research
- Streptococcal Infections and Treatments
- Bacterial biofilms and quorum sensing
- Glycosylation and Glycoproteins Research
- Caveolin-1 and cellular processes
- Galectins and Cancer Biology
- Neuropeptides and Animal Physiology
- SARS-CoV-2 and COVID-19 Research
University of Konstanz
2013-2024
University of Würzburg
2002-2007
Scripps Research Institute
1999-2003
Oregon Health & Science University
2003
Max Planck Institute for Infection Biology
1998-2002
Max Planck Society
1998-2002
Max Planck Institute for Biology
1997-1999
ABSTRACT FAK localizes to sites of transmembrane integrin receptor clustering and facilitates intracellular signaling events. FAK-null (FAK−) fibroblasts exhibit a rounded morphology, defects in cell migration, an elevated number cell-substratum contact sites. Here we show that stable re-expression epitope-tagged reversed the morphological FAK− cells through dynamic regulation actin structures focal fibronectin (FN) stimulated cells. re-expressing (clones DA2 DP3) characteristic fibrillar...
Cell migration and invasion are fundamental components of tumor cell metastasis. Increased focal adhesion kinase (FAK) expression tyrosine phosphorylation connected with elevated tumorigenesis. Null mutation FAK results in embryonic lethality, FAK−/− fibroblasts exhibit defects culture. Here we show that viral Src (v-Src) transformation cells promotes integrin-stimulated motility equal to stable reexpression. However, v-Src were not invasive, reexpression, Tyr-397 phosphorylation, activity...
The gastric pathogen <i>Helicobacter pylori</i> uses a type IV secretion system to inject the bacterial CagA protein into epithelial cells. Within host cell, becomes phosphorylated on tyrosine residues and initiates cytoskeletal rearrangements. We demonstrate here that Src-like protein-tyrosine kinases mediate phosphorylation <i>in vitro</i> vivo</i>. First, Src-specific kinase inhibitor PP2 specifically blocks rearrangements thereby inhibiting CagA-induced hummingbird phenotype of Second,...
Most transformed cells have lost anchorage and serum dependence for growth survival. Previously, we established that when is absent, fibronectin survival signals transduced by focal adhesion kinase (FAK), suppress p53-regulated apoptosis in primary fibroblasts endothelial (Ilić et al. 1998. J. Cell Biol. 143:547–560). The present goals are to identify sequences FAK signaling molecules downstream of required anchorage-dependent fibroblasts. We report binding the SH3 domain p130Cas...
Staphylococcus aureus is an important pathogen, causing a wide range of infections including sepsis, wound infections, pneumonia, and catheter-related infections. In several pathogens ClpP proteases were identified by in vivo expression technologies to be for virulence. Clp proteolytic complexes are responsible adaptation multiple stresses degrading accumulated misfolded proteins. this report clpP, encoding the subunit ATP-dependent protease, was deleted, gene DeltaclpP determined global...
Their glycolytic metabolism imposes an increased acid load upon tumour cells. The surplus protons are extruded by the Na + /H exchanger (NHE) which causes extracellular acidification. It is not yet known what mechanism pH (pH e ) and NHE activity affect cell migration thus metastasis. We studied impact of on motility human melanoma (MV3) Cells were seeded on/in collagen I matrices. Migration was monitored employing time lapse video microscopy then quantified as movement centre. Intracellular...
Nosocomial infections by Staphylococcus aureus, a Gram-positive pathogen colonising human skin and mucosal surfaces, are an increasing health care problem. Clinical isolates almost invariably express fibronectin-binding proteins that, indirectly linking the bacteria with host integrin α5β1, can promote uptake of microorganisms eukaryotic cells. Integrin engagement pathogenic S. but not non-pathogenic carnosus, triggered recruitment focal contact-associated vinculin, tensin, zyxin FAK to...
Protein glycosylation is a ubiquitous post-translational modification that involved in the regulation of many aspects protein function. In order to uncover biological roles this modification, imaging state specific proteins within living cells would be fundamental importance. To date, however, has not been achieved. Herein, we demonstrate protein-specific detection intracellular OGT, Foxo1, p53, and Akt1 cells. Our generally applicable approach relies on Diels-Alder chemistry fluorescently...
Carcinoembryonic antigen-related cell adhesion molecules (CEACAMs) are used by several human pathogens to anchor themselves or invade host cells. Interestingly, granulocytes express a specific isoform, CEACAM3, that participates together with CEACAM1 and CEACAM6 in the recognition of CEACAM-binding microorganisms. Here we show CEACAM3 can direct efficient, opsonin-independent phagocytosis Neisseria, Moraxella, Haemophilus species. CEACAM3- but not CEACAM6-mediated uptake is blocked...
Staphylococcus aureus, a common cause of nosocomial infections, is able to invade eukaryotic cells by indirectly engaging β1 integrin-containing host receptors, whereas non-pathogenic carnosus not invasive. Here, we identify intracellular signals involved in integrin-initiated internalization S. aureus. In particular, the cell actin cytoskeleton and Src family protein-tyrosine kinases (PTKs) are essential mediate aureus invasion. PTKs activated response pathogenic but carnosus. addition,...
Exfoliation, which is the detachment of infected epithelial cells, an innate defense mechanism to prevent bacterial colonization. Indeed, infection with Neisseria gonorrhoeae induced from extracellular matrix (ECM) substrate in vitro. Surprisingly, variants N. that bind human carcinoembryonic antigen-related cell adhesion molecules (CEACAMs) failed induce and, instead, promoted enhanced host ECM. Microarray analysis revealed CEACAM engagement by several pathogens triggers expression CD105....
Colonization of mucosal surfaces is the key initial step in most bacterial infections. One mechanism protecting mucosa rapid shedding epithelial cells, also termed exfoliation, but it unclear how pathogens counteract this process. We found that carcinoembryonic antigen (CEA)-binding bacteria colonized urogenital tract CEA transgenic mice, not wild-type by suppressing exfoliation cells. binding triggered de novo expression transforming growth factor receptor CD105, changing focal adhesion...