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- Function of important examples of PTK receptor families
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1. The molecular basis of insulin action
- Prof. Morris White
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2. The Eph receptor family
- Prof. Elena Pasquale
- Structure of PTK receptors and regulation of their kinases
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3. EGF receptor family: targets for improving cancer therapy
- Prof. Tony Burgess
- Intracellular signal transduction by PTK receptors
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4. PI 3-kinases and lipid messengers
- Prof. Bart Vanhaesebroeck
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5. RTKs activate the ERK 1/2 MAPK cascade
- Prof. Melanie H. Cobb
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6. The ERK1/2 MAPK cascade
- Prof. Melanie H. Cobb
- Archived Lectures *These may not cover the latest advances in the field
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7. Receptor tyrosine kinases - function, families and evolution
- Prof. Tony Hunter
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9. How the PDGF receptor induces cell proliferation
- Dr. Andrius Kazlauskas
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10. VEGF inhibitors for anti-angiogenic therapy
- Prof. Kari Alitalo
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12. Activation of PTK receptors in solid human tumors
- Dr. Marco Pierotti
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14. SH2-containing PTPs (Shps) in RTK signaling and disease
- Prof. Benjamin G. Neel
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16. Phospholipase C Gamma
- Prof. Graham Carpenter
- Ms. Cornelia Crooke
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17. Imatinib as a paradigm of targeted cancer therapies
- Prof. Brian Druker
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18. EGFR targeted therapies in lung cancer
- Dr. Pasi Janne
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19. The VEGF family
- Prof. Kari Alitalo
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20. The HGF receptor, a targettable regulator of invasive growth
- Prof. Paolo Comoglio
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21. Structural biology of FGF signaling in human development and disease
- Dr. Moosa Mohammadi
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22. EGF receptor family: targets for cancer therapeutics
- Prof. Tony Burgess
Printable Handouts
Navigable Slide Index
- Introduction
- FGF family
- Structure basic alignment of human FGF
- General FGF structure
- Why to study FGF signaling?
- Receptor tyrosine kinase family
- FGFR architecture
- Alternative splicing (AS)
- Tissue specific alternative splicing in FGFR1-3
- FGF require proteoglycans
- Structural biology of FGFR activation
- Questions to be answered
- Crystal structure of FGFR complex/FGF/heparin
- Space filling of the dimer
- The dimerization of FGFR
- The role of heparin sulfate (HP) in FGFR
- Heparin-binding canyon
- Interaction between HP and ligand or receptors
- Interactions of heparin with FGFR
- A dynamic model for generation of dimers (1)
- A dynamic model for generation of dimers (2)
- A dynamic model for generation of dimers (3)
- FGF-FGFR dimerization is cooperative process
- Different canyons of HS motifs
- FGFR autoinhibition
- D1 and the D1-D2 linker interact with D2-D3
- Molecular basis for FGF-FGFR binding specificity
- Summary of FGF-FGFR binding data
- Structure - summary
- AS in FGFR1-3 and ligand binding specificity
- FGF2 binds to receptor 2C
- FGF2-D3 interface
- FGF10 binds to FGFR2B
- FGF10-D3 interface
- Site directed mutagenesis experiments
- AS regulates tissue homeostasis-structural basis
- AS generates multiple FGF8 isoforms
- AS modulates the organizer activity of FGF8 (1)
- AS modulates the organizer activity of FGF8 (2)
- Crystal structure of FGF8b with FGFR2c
- Higher binding affinity accounts for a single residue
- Mutation reduces FGFR binding affinity of FGF8b
- Differences in patterning abilities of FGF8a/FGF8b
- Take home message
- FGF8b attains differently its binding specificity
- The unique conformation of FGF8b N-terminus
- Mechanisms of FGF-FGFR binding specificity
- D3 superimposition
- Divergent N-termini of FGF and regulation
- The conformation of FGF N-terminus differs greatly
- Structural basis for FGFR activation in disease
- Positions of various mutations
- Location of a specific mutation leads to disease
- Apert syndrome
- Crystal structure of wt and mutant receptor 2c
- Gain-of-function contacts (1)
- The superimposition of wild type FGFR2c
- Gain-of-function contacts (2)
- Apert mutations enhance the affinity
- FGF10 binds the mutant receptor
- Loss of FGFR2 binding specificity
- Pfeiffer syndrome
- Pfeiffer syndrome - FGFR2 A172F mutation
- The FGFR2 mutation
- Acknowledgments
Topics Covered
- FGF family of ligands, and FGF receptor (FGFR) subfamily of receptor tyrosine kinase superfamily
- The roles of FGF signaling in mammalian biology and diseases
- FGFR receptor alternative splicing and its essential role in epithelial-mesenchymal signaling loop, and organogenesis
- Structural mechanism by which FGF and heparan sulfate induce FGFR dimerization and activation on the cell surface
- A working model for FGFR autoinhibition
- Structural mechanisms by which FGF-FGFR binding specificity is achieved
- Structural basis for how alternative splicing regulates ligand-binding specificity of FGFRs
- Structural basis by which ligand-dependent pathogenic mutations in FGFR lead to receptor gain-of-function in human skeletal syndromes
- Structural basis by which alternative splicing regulates patterning ability of FGF8 in the brain
Links
Series:
Categories:
Talk Citation
Mohammadi, M. (2007, October 1). Structural biology of FGF signaling in human development and disease [Video file]. In The Biomedical & Life Sciences Collection, Henry Stewart Talks. Retrieved April 27, 2024, from https://hstalks.com/bs/455/.Export Citation (RIS)
Publication History
Financial Disclosures
- Dr. Moosa Mohammadi has not informed HSTalks of any commercial/financial relationship that it is appropriate to disclose.