A5051904715- Monoclonal and Polyclonal Antibodies Research
- Cell Adhesion Molecules Research
- Glycosylation and Glycoproteins Research
- Galectins and Cancer Biology
- HER2/EGFR in Cancer Research
- Peptidase Inhibition and Analysis
- Carbohydrate Chemistry and Synthesis
- Biochemical and Structural Characterization
- Caveolin-1 and cellular processes
- Signaling Pathways in Disease
University of Copenhagen
2015-2024
Mutations in the TMEM260 gene cause structural heart defects and renal anomalies syndrome, but function of encoded protein remains unknown. We previously reported wide occurrence O-mannose glycans on extracellular immunoglobulin, plexin, transcription factor (IPT) domains found hepatocyte growth receptor (cMET), macrophage-stimulating (RON), plexin receptors, further demonstrated that two known O-mannosylation systems orchestrated by POMT1/2 transmembrane tetratricopeptide repeat-containing...
The metalloproteinase ADAM17 activates ErbB signalling by releasing ligands from the cell surface, a key step underlying epithelial development, growth and tumour progression. However, mechanisms acutely controlling cell-surface availability to modulate extent of ligand release are poorly understood. Here, through functional genome-wide siRNA screen, we identify sorting protein PACS-2 as regulator trafficking signalling. loss reduces levels ADAM17-dependent shedding, without apparent effects...
Desmoplasia is a common feature of aggressive cancers, driven by complex interplay protein production and degradation. Basigin type 1 integral membrane receptor secreted in exosomes or released ectodomain shedding from the cell surface. Given that soluble basigin increased circulation patients with poor cancer prognosis, we explored putative role ADAM12-generated progression. We show recombinant binds β1 integrin stimulates gelatin degradation migration cells matrix metalloproteinase (MMP)-...
ABSTRACT The transmembrane protease ADAM9 is frequently upregulated in human cancers, and it promotes tumour progression mice. In vitro, regulates cancer cell adhesion migration by interacting with integrins. However, how modulates integrin functions not known. We here show that knockdown increases β1 levels through mechanisms are independent of its activity. ADAM9-silenced cells, to collagen fibronectin reduced, suggesting an altered function the accumulated Mechanistically,...
Abstract Mutations in the TMEM260 gene cause structural heart defects and renal anomalies syndrome (SHDRA), but function of encoded protein remains unknown. We report that is an ER-located O-mannosyltransferase selectively glycosylates defined extracellular immunoglobulin, plexin, transcription factor (IPT) domains hepatocyte growth receptor (cMET), macrophage-stimulating (RON), plexin receptors. demonstrate disease-causing mutations impair O-mannosylation IPT knock out cells results...