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Fibroblast growth factor receptor 3

FGFR3, fibroblast growth factor receptor 3
This gene encodes a member of the fibroblast growth factor receptor (FGFR) family, with its amino acid sequence being highly conserved between members and among divergent species. FGFR family members differ from one another in their ligand affinities and tissue distribution. A full-length representative protein would consist of an extracellular region, composed of three immunoglobulin-like domains, a single hydrophobic membrane-spanning segment and a cytoplasmic tyrosine kinase domain. The extracellular portion of the protein interacts with fibroblast growth factors, setting in motion a cascade of downstream signals, ultimately influencing mitogenesis and differentiation. This particular family member binds acidic and basic fibroblast growth hormone and plays a role in bone development and maintenance. Mutations in this gene lead to craniosynostosis and multiple types of skeletal dysplasia. Three alternatively spliced transcript variants that encode different protein isoforms have been described. [provided by RefSeq, Jul 2009] (from NCBI)
Top mentioned proteins: CAN, HAD, FGFR1, p53, FGFR2
Papers using FGFR3 antibodies
G protein-coupled receptor endocytosis in ADP-ribosylation factor 6-depleted cells.
Keen James, In PLoS ONE, 2004
... KY); mouse anti-CHC (RDI division of Fitzgerald Industries, Concorde, MA); goat anti-CHC, rabbit anti-FGFR1, rabbit anti-FGFR3 (Santa Cruz Biotechnology, Santa Cruz, CA); rabbit ...
Papers on FGFR3
FGF9 and FGF18 in idiopathic pulmonary fibrosis promote survival and migration and inhibit myofibroblast differentiation of human lung fibroblasts in vitro.
Mailleux et al., Paris, France. In Am J Physiol Lung Cell Mol Physiol, Feb 2016
FGFR3 was generally detected in fibroblast foci by immunohistochemistry.
Genomic Biomarkers for the Prediction of Stage and Prognosis of Upper Tract Urothelial Carcinoma.
Coleman et al., New York City, United States. In J Urol, Feb 2016
RESULTS: Of the 24 most commonly altered genes within 9 pathways, TP53/MDM2 alterations and FGFR3 mutations were the only two alterations uniformly associated with high-grade, advanced stage, non-organ-confined disease, recurrence-free survival, and cancer-specific survival.
Muenke syndrome: An international multicenter natural history study.
Muenke et al., Würzburg, Germany. In Am J Med Genet A, Feb 2016
Muenke syndrome constitutes the most common syndromic form of craniosynostosis, with an incidence of 1 in 30,000 births and is defined by the presence of the p.Pro250Arg mutation in FGFR3.
Altered FGF signalling in congenital craniofacial and skeletal disorders.
Wollnik et al., Göttingen, Germany. In Semin Cell Dev Biol, Jan 2016
In humans, four FGFRs are described, and, to date, mutations in FGFR1, FGFR2, and FGFR3 have been shown to underlie human developmental disorders.
Mechanism of FGF receptor dimerization and activation.
Hristova et al., Baltimore, United States. In Nat Commun, Dec 2015
The pathogenic A391E mutation in FGFR3 TM domain emulates the action of fgf2, trapping the FGFR3 dimer in its most active state.
C-Type Natriuretic Peptide Analog as Therapy for Achondroplasia.
Legeai-Mallet, Paris, France. In Endocr Dev, Dec 2015
Fibroblast growth factor receptor 3 (FGFR3) is an important regulator of bone formation.
[Recent advances in bladder urothelial carcinogenesis].
Bieche et al., Marseille, France. In Bull Cancer, Dec 2015
Main molecular alterations concern FGFR3, TP53 and HER2, and it is now possible to distinguish three subgroups of tumors according to molecular profile.
Fibroblast Growth Factor Receptors: From the Oncogenic Pathway to Targeted Therapy.
Varella-Garcia et al., Aurora, United States. In Curr Mol Med, Dec 2015
DNA and RNA-based technologies have been used to detect these abnormalities, especially in FGFR1, FGFR2 and FGFR3 and tests have been developed for their detection, but no assay has been proved ideal for molecular diagnosis.
Mutational Spectrum, Copy Number Changes, and Outcome: Results of a Sequencing Study of Patients With Newly Diagnosed Myeloma.
Morgan et al., Newcastle upon Tyne, United Kingdom. In J Clin Oncol, Dec 2015
RESULTS: We identified 15 significantly mutated genes: IRF4, KRAS, NRAS, MAX, HIST1H1E, RB1, EGR1, TP53, TRAF3, FAM46C, DIS3, BRAF, LTB, CYLD, and FGFR3.
Phase I Dose-Escalation Study of JNJ-42756493, an Oral Pan-Fibroblast Growth Factor Receptor Inhibitor, in Patients With Advanced Solid Tumors.
Soria et al., Madrid, Spain. In J Clin Oncol, Nov 2015
Among 23 response-evaluable patients with tumor FGFR pathway alterations, four confirmed responses and one unconfirmed partial response were observed in patients with glioblastoma and urothelial and endometrial cancer (all with FGFR2 or FGFR3 translocations); 16 patients had stable disease.
Non-muscle invasive bladder cancer risk stratification.
Konety et al., Minneapolis, United States. In Indian J Urol, Oct 2015
Molecular biomarkers such as Ki-67, FGFR3 and p53 appear to be promising in predicting recurrence and progression but need further validation prior to using them in clinical practice.
Characterization of membrane protein interactions in plasma membrane derived vesicles with quantitative imaging Förster resonance energy transfer.
Hristova et al., Baltimore, United States. In Acc Chem Res, Sep 2015
We focus on the dimerization of fibroblast growth factor receptor 3 (FGFR3), a RTK that plays a critically important role in skeletal development.
Patient-derived models of acquired resistance can identify effective drug combinations for cancer.
Engelman et al., Boston, United States. In Science, 2015
For example, the combination of ALK and MAPK kinase (MEK) inhibitors was active in an ALK-positive resistant tumor that had developed a MAP2K1 activating mutation, and the combination of EGFR and fibroblast growth factor receptor (FGFR) inhibitors was active in an EGFR mutant resistant cancer with a mutation in FGFR3.
Whole-exome sequencing and whole genome re-sequencing for prenatal diagnosis of achondroplasia.
Wang et al., Beijing, China. In Int J Clin Exp Med, 2014
WES was conducted to determine the mutation of fibroblast growth factor receptor 3 (FGFR3) gene in one special family with rickets and dwarfism.
Statin treatment rescues FGFR3 skeletal dysplasia phenotypes.
Tsumaki et al., Kyoto, Japan. In Nature, 2014
Gain-of-function mutations in the fibroblast growth factor receptor 3 gene (FGFR3) result in skeletal dysplasias, such as thanatophoric dysplasia and achondroplasia (ACH).
Transforming fusions of FGFR and TACC genes in human glioblastoma.
Iavarone et al., New York City, United States. In Science, 2012
study reports that a small subset of glioblastoma multiforme tumors harbors oncogenic chromosomal translocations that fuse in-frame the tyrosine kinase coding domains of fibroblast growth factor receptor genes(FGFR1 or FGFR3) to the transforming acidic coiled-coil coding domains of TACC1 or TACC3; the FGFR-TACC fusion protein displays oncogenic activity
Reactivation of mitogen-activated protein kinase (MAPK) pathway by FGF receptor 3 (FGFR3)/Ras mediates resistance to vemurafenib in human B-RAF V600E mutant melanoma.
Peng et al., Indianapolis, United States. In J Biol Chem, 2012
Reactivation of mitogen-activated protein kinase (MAPK) pathway by FGF receptor 3 (FGFR3)/Ras mediates resistance to vemurafenib in human B-RAF V600E mutant melanoma.
CDKN2A homozygous deletion is associated with muscle invasion in FGFR3-mutated urothelial bladder carcinoma.
Radvanyi et al., Paris, France. In J Pathol, 2012
Highlight the crucial role of CDKN2A loss in the progression of non-muscle-invasive FGFR3-mutated bladder carcinomas and provide a potentially useful clinical marker for adapting the treatment of such tumours.
Muenke syndrome mutation, FgfR3P²⁴⁴R, causes TMJ defects.
Koyama et al., Philadelphia, United States. In J Dent Res, 2012
activating FgfR3(P244R) mutation disturbs temporomandibular joint developmental processes, likely by reducing hedgehog signaling and endochondral ossification
Effect of the G375C and G346E achondroplasia mutations on FGFR3 activation.
Hristova et al., Baltimore, United States. In Plos One, 2011
We find that this mutation does not increase FGFR3 phosphorylation and decreases FGFR3 cross-linking propensity, a finding which raises questions whether this mutation is indeed a genetic cause for human dwarfism.
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