Manuel Koch

This study identifies SVEP1 as a mediator of ANG2-TIE1 binding, leading to TIE1 phosphorylation and downstream signaling in lymphatic endothelial cells.

The paper identifies gH/UL116 as a target for antibodies that neutralize HCMV and activate FcγR, showing its potential as a vaccine candidate.

The paper identifies a broadly neutralizing antibody against multiple orthoebolaviruses from an rVSV-EBOV vaccinated individual and shows its protective efficacy in animal models.

This study uses cryo-EM to analyze antibodies targeting HCMV glycoproteins, identifying synergistic combinations that enhance neutralization.

This study identifies TANGO1 as a selective ECM cargo receptor that directly recognizes specific collagen and fibrillin isoforms through a conserved tyrosine residue, independent of HSP47.

This study shows that the balance between TNX and TNC, controlled by TGF-β, affects tumor cell proliferation in pancreatic cancer, suggesting TNX as a potential therapeutic target.

The paper examines differences in mononuclear cells and myonuclei at human myofibre tips, finding more mononuclear cells and COL22A1-expressing nuclei in type II fibres compared to type I.

The paper identifies Collagen XV-B and Tenascin C as ECM components guiding motor axon growth through their dual topology and stiffness in zebrafish.

This study identifies a genetic interaction between svep1 and tie1 in zebrafish lymphatic development, independent of Vegfc, and links it to human glaucoma.

The paper uses single nucleus RNA-seq to identify distinct myonuclei profiles at the human myotendinous junction, revealing gene expression patterns and subclusters associated with specific proteins and fibre types.

This study shows that collagen XII deficiency in mice causes patella dislocation and myopathy, with altered gene expression in tenocytes and human patients showing similar patella instability.

The paper identifies ALPK1 and TIFA as key components of an innate immune response triggered by H. pylori's T4SS, independent of CagA translocation.