ArticleBiochimica et biophysica acta2011
The A391E mutation enhances FGFR3 activation in the absence of ligand.
Article in Biochimica et biophysica acta, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 29 citations in OpenAlex.
- Towards generalizable predictions for G protein-coupled receptor variant expression.Biophysical journal · 2022Article
- FGFR3 overactivation in the brain is responsible for memory impairments in Crouzon syndrome mouse model.The Journal of experimental medicine · 2022Article
- ETV5 links the FGFR3 and Hippo signalling pathways in bladder cancer.Scientific reports · 2019Article
- Molecular investigation of FGFR3 gene mutation and its correlation with clinicopathological findings in Indian bladder cancer patients.Cancer reports (Hoboken, N.J.) · 2018Article
- Pathogenic Cysteine Removal Mutations in FGFR Extracellular Domains Stabilize Receptor Dimers and Perturb the TM Dimer Structure.Journal of molecular biology · 2016Article
- Effect of the achondroplasia mutation on FGFR3 dimerization and FGFR3 structural response to fgf1 and fgf2: A quantitative FRET study in osmotically derived plasma membrane vesicles.Biochimica et biophysica acta · 2016Article
- Mechanism of FGF receptor dimerization and activation.Nature communications · 2016Article
- Characterization of membrane protein interactions in plasma membrane derived vesicles with quantitative imaging Förster resonance energy transfer.Accounts of chemical research · 2015Article
- The safety dance: biophysics of membrane protein folding and misfolding in a cellular context.Quarterly reviews of biophysics · 2015Article
- Coupling of transmembrane helix orientation to membrane release of the juxtamembrane region in FGFR3.Biochemistry · 2014Article
- FGFR3 transmembrane domain interactions persist in the presence of its extracellular domain.Biophysical journal · 2013Article
- The pathogenic A391E mutation in FGFR3 induces a structural change in the transmembrane domain dimer.The Journal of membrane biology · 2013Article
- Multiple consequences of a single amino acid pathogenic RTK mutation: the A391E mutation in FGFR3.PloS one · 2013Article
- Structural differences between thermophilic and mesophilic membrane proteins.Protein science : a publication of the Protein Society · 2012Article
- p38 Inhibition ameliorates skin and skull abnormalities in Fgfr2 Beare-Stevenson mice.The Journal of clinical investigation · 2012Article
- Physical-chemical principles underlying RTK activation, and their implications for human disease.Biochimica et biophysica acta · 2012Review
- A Decade of FGF Receptor Research in Bladder Cancer: Past, Present, and Future Challenges.Advances in urology · 2012Article
- Direct assessment of the effect of the Gly380Arg achondroplasia mutation on FGFR3 dimerization using quantitative imaging FRET.PloS one · 2012Article
- Article
- The physical basis of FGFR3 response to fgf1 and fgf2.Biochemistry · 2011Article
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
The A391E mutation in the transmembrane domain of fibroblast growth factor receptor 3 leads to aberrant development of the cranium. It has been hypothesized that the mutant glutamic acid stabilizes the dimeric receptor due to hydrogen bonding and enhances its ligand-independent activation. We previously tested this hypothesis in lipid bilayers and showed that the mutation stabilizes the isolated transmembrane domain dimer by -1.3°kcal/mol. Here we further test the hypothesis, by investigating the effect of the A391E mutation on the activation of full-length fibroblast growth factor receptor 3 in human embryonic kidney 293T cells in the absence of ligand. We find that the mutation enhances the ligand-independent activation propensity of the receptor by -1.7°kcal/mol. This value is consistent with the observed strength of hydrogen bonds in membranes, and supports the above hypothesis.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.