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Structural basis for a direct interaction between FGFR1 and NCAM and evidence for a regulatory role of ATP.
It is demonstrated for the first time a direct interaction between NCAM and FGFR1 andFGFR1 by surface plasmon resonance (SPR) analysis and it is demonstrated that the NCAM module was able to induce activation (phosphorylation) of FGFR and to stimulate neurite outgrowth induced by the module. Expand
Neural Cell Adhesion Molecule-Stimulated Neurite Outgrowth Depends on Activation of Protein Kinase C and the Ras–Mitogen-Activated Protein Kinase Pathway
It is proposed that PKC serves as the link between the two pathways activating Raf and thereby creating the sustained activity of the MAP kinases necessary for neuronal differentiation, and this model of NCAM signaling involving two pathways is proposed. Expand
Structure and interactions of NCAM Ig1-2-3 suggest a novel zipper mechanism for homophilic adhesion.
A novel model for NCAM homophilic binding is presented, which results in two perpendicular zippers forming a double zipper-like NCAM adhesion complex. Expand
The binding of NCAM to FGFR1 induces a specific cellular response mediated by receptor trafficking
Although FGF-2 causes the FGFR to be internalized and degraded, NCAM gets cells moving by stabilizing the receptor, promoting receptor recycling, and initiating a promigratory signaling cascade.
Structural biology of NCAM homophilic binding and activation of FGFR
Evidence is provided that FGFR is probably activated by NCAM very differently from the way by which it is activated by FGFs, reflecting the different conditions for NCAM-FGFR and FGF–FGFR interactions. Expand
Regulators of Neurite Outgrowth: Role of Cell Adhesion Molecules
The structure, function, and signaling of three key CAMs found in the nervous system are described: N‐cadherin and two Ig‐CAMs, L1 and the neural cell adhesion molecule NCAM. Expand
Zippers Make Signals: NCAM-mediated Molecular Interactions and Signal Transduction
The neural cell adhesion molecule, NCAM, is involved in multiple cis- and trans-homophilic interactions (NCAM binding to NCAM) thereby facilitating cell–cell adhesion through the formation ofExpand
TLR4 links podocytes with the innate immune system to mediate glomerular injury.
TLR4 is constitutively expressed by podocytes and is upregulated in MPGN, where it may mediate glomerular injury by modulating expression of chemokines; therefore, TLR4 may link podocytes with the innate immune system to mediate MPGN triggered by the deposition of immune complexes. Expand
Novel role of toll-like receptor 3 in hepatitis C-associated glomerulonephritis.
It is hypothesized that immune complexes containing viral RNA activate mesangial TLR3 during HCV infection, thereby contributing to chemokine/cytokine release and effecting proliferation and apoptosis and establishing a link between viral infections and glomerular diseases. Expand
Neural cell adhesion molecule function is regulated by metalloproteinase‐mediated ectodomain release
It is demonstrated that NCAM can be released from primary hippocampal neurons in culture and that metalloproteinase‐dependent shedding of NCAM regulates NCAM‐mediated neurite outgrowth, suggesting that membrane‐bound NC AM can be cleaved extracellularly by a metallobroteinase. Expand