ArticleCellular signalling2008
Sprouty 2 disturbs FGFR3 degradation in thanatophoric dysplasia type II: a severe form of human achondroplasia.
Article in Cellular signalling, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
18 citing papers in PubMed, 32 citations in OpenAlex.
- Sprouty2 Regulates Endocytosis and Degradation of Fibroblast Growth Factor Receptor 1 in Glioblastoma Cells.Cells · 2024Article
- FGFR-targeted therapeutics: clinical activity, mechanisms of resistance and new directions.Nature reviews. Clinical oncology · 2024Review
- Association ofGenes · 2024Article
- Review
- Current Care and Investigational Therapies in Achondroplasia.Current osteoporosis reports · 2017Review
- Identification of therapeutic targets for Parkinson's disease via bioinformatics analysis.Molecular medicine reports · 2017Article
- Article
- Fibroblast growth factor signaling in myofibroblasts differs from lipofibroblasts during alveolar septation in mice.American journal of physiology. Lung cellular and molecular physiology · 2015Article
- Article
- Structural mimicry of a-loop tyrosine phosphorylation by a pathogenic FGF receptor 3 mutation.Structure (London, England : 1993) · 2013Article
- Sixteen years and counting: the current understanding of fibroblast growth factor receptor 3 (FGFR3) signaling in skeletal dysplasias.Human mutation · 2012Review
- The physical basis of FGFR3 response to fgf1 and fgf2.Biochemistry · 2011Article
- Fibroblast growth factor receptor 3 (FGFR3) is a strong heat shock protein 90 (Hsp90) client: implications for therapeutic manipulation.The Journal of biological chemistry · 2011Article
- The ubiquitin-proteasomal system is critical for multiple myeloma: implications in drug discovery.American journal of blood research · 2011Article
- HECT domain-containing E3 ubiquitin ligase Nedd4 interacts with and ubiquitinates Sprouty2.The Journal of biological chemistry · 2010Article
- The development of the thalamic motor learning area is regulated by Fgf8 expression.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2009Article
- Intermolecular interactions of Sprouty proteins and their implications in development and disease.Molecular pharmacology · 2009Review
- An expressed fgf4 retrogene is associated with breed-defining chondrodysplasia in domestic dogs.Science (New York, N.Y.) · 2009Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 3 institutions in 1 country.
Funding
Abstract
Thanatophoric dysplasia is a member of the achondroplasia family of human skeletal dysplasias, which result from FGFR3 mutations that exaggerate this receptor's inhibitory influence on chondrocyte proliferation and differentiation in the skeletal growth plate. We have previously reported that defective lysosomal degradation of activated receptor contributes to the gain-of-function of the mutant FGFR3. We now provide evidence that this disturbance is mediated by the receptor's kinase activity and involves constitutive induction and activation of Spry2. Our findings suggest that activated Spry2 may interfere with c-Cbl-mediated ubiquitination of FGFR3 by sequestering c-Cbl. They provide novel insight into the pathogenesis of this group of human skeletal dysplasias and identify a mechanism that potentially could be targeted therapeutically.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
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.