Structural basis for fibroblast growth factor receptor activation.
By M. Mohammadi, S. Olsen, O. Ibrahimi. Cytokine & growth factor reviews, 2005
763 citations recorded by the source corpus.
Subfields: Cell Biology, Genetics, Molecular Biology
View Paper: https://www.semanticscholar.org/paper/6a49b9abbdfacd58d741396d8fe33e4347f5ec2e
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Citations in the corpus
- Heparan sulphate proteoglycans fine-tune mammalian physiology (2007, background): “The interaction of heparin and HS with FGFs and their receptors has also been characterized in great detai”
- Regulation of Phosphate Homeostasis by PTH, Vitamin D, and FGF23 (2010, background): “Lack of HS binding-motifs reduces matrix-binding and enables this ligand to function in an endocrine fashion (69).”
- The FGF family: biology, pathophysiology and therapy (2009, neutral): “In general, primary sequence variation of the N- and C-terminal tails of FGFs accounts for the different biology of the ligand”
- Fibroblast growth factor signalling: from development to cancer (2010, background): “Cell surface HPSGs also stabilize the FGF ligand–receptor interaction, forming a ternary complex with FGF”
- Demystifying Heparan Sulfate–Protein Interactions (2014, background): “Many members of the FGF family interact with HS and form dimers (47, 48).”
- Osteoarthritis: pathogenic signaling pathways and therapeutic targets (2023, background): “At the same time, FGFs 1, 2, 5, 8, 9, 16–19, 21, and 23 are expressed in the growth plate chondrocytes, and FGFs 1, 2, 6, 7, 9, 18, 21, and 22 are expressed in the perichondrium.(366) Previous studies have shown that FGFs 1, 2, 7, 8, 9,18, and 23 are the major ones associated with the pathogenesis o”
- Research resource: Comprehensive expression atlas of the fibroblast growth factor system in adult mouse. (2010, background): “These interactions are necessary for efficient FGF-FGFR binding and dimerization (8).”