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Fibroblast growth factor receptor 2

FGFR2, FGF receptor, fibroblast growth factor receptor 2
The protein encoded by this gene is a member of the fibroblast growth factor receptor family, where amino acid sequence is highly conserved between members and throughout evolution. FGFR family members differ from one another in their ligand affinities and tissue distribution. A full-length representative protein consists 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 is a high-affinity receptor for acidic, basic and/or keratinocyte growth factor, depending on the isoform. Mutations in this gene are associated with Crouzon syndrome, Pfeiffer syndrome, Craniosynostosis, Apert syndrome, Jackson-Weiss syndrome, Beare-Stevenson cutis gyrata syndrome, Saethre-Chotzen syndrome, and syndromic craniosynostosis. Multiple alternatively spliced transcript variants encoding different isoforms have been noted for this gene. [provided by RefSeq, Jan 2009] (from NCBI)
Top mentioned proteins: FGFR1, CAN, Fibroblast Growth Factor 2, V1a, HAD
Papers using FGFR2 antibodies
Radial migration of superficial layer cortical neurons controlled by novel Ig cell adhesion molecule MDGA1.
Maas Stefan, In PLoS ONE, 2005
... The FGFR2 genomic region spanning from exon 7 to exon 10 from mouse genomic DNA was amplified by PCR and cloned into Gateway Destination vector (Invitrogen), carrying both EGFP (Clontech) and mRFP ...
Papers on FGFR2
FGFR Inhibitor Ameliorates Hypophosphatemia and Impaired Engrailed-1/Wnt Signaling in FGF2 High Molecular Weight Isoform Transgenic Mice.
Hurley et al., Farmington, United States. In J Cell Biochem, Feb 2016
Since abnormal Wnt signaling was reported in Hyp mice we assessed whether Wnt signaling was impaired in HMWTg kidneys and the effect of blocking FGF receptor (FGFR) signaling.
Association between insulin resistance and impairment of FGF21 signal transduction in skeletal muscles.
Lee et al., Suwŏn, South Korea. In Endocrine, Feb 2016
Levels of FGF21 increased, whereas levels of phosphorylated FGF receptor (p-FGFR), phosphorylated FGFR substrates 2α (p-FRS2α), and phosphorylated extracellular signal-regulated kinases (p-ERK) decreased in the skeletal muscle of both T2DM patients and IGT subjects.
Endothelial Fibroblast Growth Factor Receptor signaling is required for vascular remodeling following cardiac ischemia-reperfusion injury.
Ornitz et al., Saint Louis, United States. In Am J Physiol Heart Circ Physiol, Feb 2016
To determine the requirement for FGFR signaling in endothelium in cardiac ischemia-reperfusion injury, we conditionally inactivated the Fgfr1 and Fgfr2 genes in endothelial cells with Tie2-Cre (Tie2-Cre, Fgfr1(f/f), Fgfr2(f/f) DCKO mice).
Gene-based analysis of the fibroblast growth factor receptor signaling pathway in relation to breast cancer in African American women: the AMBER consortium.
Palmer et al., Boston, United States. In Breast Cancer Res Treat, Feb 2016
UNASSIGNED: We conducted gene-based analysis in 26 genes in the FGFR signaling pathway to identify genes carrying genetic variation affecting risk of breast cancer and the specific estrogen receptor (ER) subtypes.
Fibroblast growth factors, old kids on the new block.
Wang et al., Wenzhou, China. In Semin Cell Dev Biol, Feb 2016
The family includes canonic FGFs that elicit their activities by activating the FGF receptor (FGFR) tyrosine kinase and non-canonic members that elicit their activities intracellularly and via FGFR-independent mechanisms.
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.
The role of mutations and overexpression of the fibroblast growth factor receptor-3 in bladder cancer.
Zhang et al., Jining, China. In Minerva Med, Dec 2015
FGF receptor (FGFR) 3 may thus serve as a promising biomarker for BC.
Association of polymorphisms with a family history of cancer and the presence of germline mutations in the BRCA1/BRCA2 genes.
Palmero et al., Barretos, Brazil. In Hered Cancer Clin Pract, Dec 2015
The constitutive DNA was analyzed for the presence of polymorphisms at rs2981582 (FGFR2 gene); rs3803662 (TNRC9); rs889312 (MAP3K1); rs3817198 (LSP1 gene); and rs13281615 (8q24).
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.
Dysregulated FGF signalling in neoplastic disorders.
Grose et al., London, United Kingdom. In Semin Cell Dev Biol, Nov 2015
Dissection of the mechanisms that underlie the pro-tumourigenic effects resulting from perturbations to the FGF signalling network will be of utmost importance to the development of therapeutic approaches to treat FGF receptor (FGFR)-driven cancers.
Genomic spectra of biliary tract cancer.
Shibata et al., Tokyo, Japan. In Nat Genet, Sep 2015
Gene fusions involving FGFR2 and PRKACA or PRKACB preferentially occurred in ICC and ECC, respectively, and the subtype-associated prevalence of actionable growth factor-mediated signals was noteworthy.
Long-Pentraxin 3 Derivative as a Small-Molecule FGF Trap for Cancer Therapy.
Presta et al., Brescia, Italy. In Cancer Cell, Sep 2015
The fibroblast growth factor (FGF)/FGF receptor (FGFR) system plays a crucial role in cancer by affecting tumor growth, angiogenesis, drug resistance, and escape from anti-angiogenic anti-vascular endothelial growth factor therapy.
Second-line dovitinib (TKI258) in patients with FGFR2-mutated or FGFR2-non-mutated advanced or metastatic endometrial cancer: a non-randomised, open-label, two-group, two-stage, phase 2 study.
Kristeleit et al., Los Angeles, United States. In Lancet Oncol, Jun 2015
BACKGROUND: Activating FGFR2 mutations are found in 10-16% of primary endometrial cancers and provide an opportunity for targeted therapy.
Ameloblastoma: A Review of Recent Molecular Pathogenetic Discoveries.
Betz et al., Ann Arbor, United States. In Biomark Cancer, 2014
The discovery of recurrent activating mutations in FGFR2, BRAF, and RAS in a large majority of ameloblastomas has implicated dysregulation of MAPK pathway signaling as a critical step in the pathogenesis of this tumor.
Anchored multiplex PCR for targeted next-generation sequencing.
Le et al., Boston, United States. In Nat Med, 2014
On the basis of our experience with performing AMP on 986 clinical FFPE samples, we show its potential as both a robust clinical assay and a powerful discovery tool, which we used to identify new therapeutically important gene fusions: ARHGEF2-NTRK1 and CHTOP-NTRK1 in glioblastoma, MSN-ROS1, TRIM4-BRAF, VAMP2-NRG1, TPM3-NTRK1 and RUFY2-RET in lung cancer, FGFR2-CREB5 in cholangiocarcinoma and PPL-NTRK1 in thyroid carcinoma.
Fibroblast growth factor receptor 2 homodimerization rapidly reduces transcription of the pluripotency gene Nanog without dissociation of activating transcription factors.
Terada et al., Gainesville, United States. In J Biol Chem, 2012
FGFR2 induces rapid but reversible Nanog repression within ES cells.
A Sox9/Fgf feed-forward loop maintains pancreatic organ identity.
Sander et al., San Diego, United States. In Development, 2012
Results demonstrate that organ fate commitment and progenitor cell expansion are coordinately controlled by the activity of a Sox9/Fgf10/Fgfr2b feed-forward loop in the pancreatic niche.
Mesodermal expression of Fgfr2S252W is necessary and sufficient to induce craniosynostosis in a mouse model of Apert syndrome.
Basilico et al., New York City, United States. In Dev Biol, 2012
Data show that fibroblast growth factor receptor 2 Fgfr2(S252W) mutation of the mesoderm alone is necessary and sufficient to cause craniosynostosis.
Syndromic craniosynostosis, fibroblast growth factor receptor 2 (FGFR2) mutations, and sacrococcygeal eversion presenting as human tails.
Winston et al., Aurora, United States. In Childs Nerv Syst, 2012
increased FGFR2 activation during this embryonic period leads to abnormal differentiation or regression of the tail bud and, in turn, sacrococcygeal eversion, in certain patients with severe syndromic craniosynostosis
Inhibition of basal FGF receptor signaling by dimeric Grb2.
Ladbury et al., Houston, United States. In Cell, 2012
Study describes a mechanism whereby Grb2 exerts control of FGFR2 kinase activity prior to growth factor binding.
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