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Results suggest that fibroblast growth factor receptor 2 (FGFR2) expression might be negatively regulated by neurofibromin 2 (NF2) signaling in the mesothelial cells.
Downregulation of circular RNA UVRAG (circUVRAG suppressed fibroblast growth factor receptor 2 (FGFR2) expression by targeting miR-223.
The results showed no association between two SNPs, rs1219648 and rs2981582, and breast cancer risk, although in a stratified analysis rs2981582 strongly associated with premenopausal and ER-positive breast cancer in Chinese patients.
The consequent appearance of the mesenchymal FGFR2c variant in the epithelial context would drive early steps of carcinogenesis.
FGFR2 was shown to be markedly overexpressed in gastric cancer tissues and correlated with a high risk of lymph node metastasis and late clinical stage. FGFR2 was negatively associated with TSP4 and FGFR2 activation could downregulate TSP4 expression, which played an important role in the proliferation, invasion and migration of gastric cancer cells.
In male breast cancer, smoking habits had a significant effect on overall survival at 10 years. In the same multivariate analysis, we found a significantly higher overall survival in cases with FGFR2 rs2981582 variant in the dominant transmission model A sensitivity analysis with left truncation showed similar results.
Results showed that HER2 and FGFR2 are regulated by DDX6 at the post-transcriptional step in gastric cancer.
High FGFR2 expression is associated with epithelial ovarian cancer cell proliferation and invasion.
There is a wide spectrum of mutations in FGFR2 shown to be causative for Pfeiffer syndrome. Here we report the first Chinese three-generation family with FGFR2 mutation c.514_515delGCinsTT (p.Ala172Phe).
It was concluded that miR494 inhibited the cancer initiating cells phenotype and reversed resistance to lapatinib by inhibiting FGFR2 in HER2positive gastric cancer.
Patients with very strong FGFR2 mRNA expression showed more homogeneous FGFR2 mRNA expression compared to patients with lower FGFGR2 mRNA expression
Findings suggest that excessive KGF and KGFR synthesis may contribute to the hyperproliferative state in cholesteatoma and could explain the pathological difference between cholesteatoma and CSOM.
provide a comprehensive update on FGFR2-related syndromic craniosynostosis
The mutations were not present in any of the unaffected family members or unrelated control subjects. These findings expand the mutation spectrum of FGFR2, and are valuable for genetic counseling in addition to prenatal diagnosis in patients with Crouzon syndrome.
Fibroblast growth factor receptor 2 (FGFR2) splice site variants were identified in eight patients with Crouzon or Pfeiffer syndrome.
Data suggest that the SOX9 transcription factor (SOX9)-fibroblast growth factor receptor 2 (FGFR2b) feed-forward loop has a lineage dependency role in pancreatic ductal adenocarcinoma (PDAC).
this study reports for the first time the p.W290G mutation in patients with PS. Based on clinical features, genetic, and computational analysis and genotype-phenotype association studies
Studies indicate that switching from fibroblast growth factor receptor 2 (FDFR-2) IIIb to IIIc variants correlates with the aggressiveness of the cancers via epithelial-mesenchymal transition [Review].
These results unveil the complexity of ER regulation by FGFR2-mediated signaling likely to be associated with BCa resistance to endocrine therapy.
Study report that 5-10% of epidermal nevi harbor embryonic postzygotic FGFR2 activating mutations.
During embryogenesis, SOX9-positive (+) cells inside hair follicles, which were previously known to give rise to hair follicle stem cells (HFSCs) and cells of the hair follicle lineage, can also give rise to Merkel Cells. Interestingly, while SOX9 is critical for HFSC specification, it is dispensable for Merkel cell formation. Conversely, FGFR2 is required for Merkel cell formation but is dispensable for HFSCs.
Fgfr2 mediated FGF signaling in palate mesenchymal cells is functionally required for palate development at various stages including a possible role in shelf initiation out of the maxillary process on E11.5.
gain-of-function mutation in FGFR2 exerts a Wnt/beta-catenin-dependent anabolic effect on trabecular bone by promoting bone formation.
small interfering RNA knockdown of FGFR2 suppressed PI3K/Akt pathway activation by FGF10 and abolished its anti-apoptotic and neurite repair effects in vitro.
Testis determination involves FGFR2c-mediated repression of both the WNT4- and FOXL2-driven ovarian-determining pathways.
The results of this study showed that GF22KO mice display longer duration of floating and decreased latency to float in the forced swim test, increased immobility in the tail suspension test, and decreased preference for sucrose in the sucrose preference test, which are all suggestive of a depressive-like phenotype.
the localization of FGF9 and its receptors at different embryonic and postnatal stages in mice testes, was examined.
FGFR2 signalling correlates with maintenance of expression of a key transcription factor for basal cell self-renewal and differentiation: SOX2.
Fgfr2 is seen within submucosal glandular epithelial cells. The medial nasal glands were missing in Fgfr2b mutants.
It is well accepted that myelin is a biologically active membrane in active communication with the axons. However, the axonal signals, the receptors on myelin, and the integration of intracellular signaling pathways emanating downstream from these receptors that drive the growth of the myelin sheath remain poorly understood in the CNS. This study brings up the intriguing possibility that FGF receptor 2, in the oligodendr
data suggest that FGF2 levels are critically related to anxiety behavior and hypothalamic pituitary- adrenal axis activity, likely through modulation of hippocampal glucocorticoid receptor expression, an effect that is likely receptor mediated, albeit not by FGFR1, FGFR2, and FGFR3.
Results show that Fgfr2 regulates both the formation and resolution of tetrads and rosettes in the mouse embryo, possibly in part by spatially restricting atypical protein kinase C, a negative regulator of non-muscle myosin IIB.
FGFR2c signaling regulates branching morphogenesis through the activation of FGFR2b signaling via increased FGF10 autocrine. These results provide new insight into the mechanisms by which crosstalk between FGFR2b and FGFR2c results in efficient branching morphogenesis.
Fgfr2 is critical for bladder mesenchyme patterning by virtue of its role in modulation of hedgehog signaling
Ectopic expression of Fgfr2c was detected within the affected sutures of Bcl11b(-/-) mice. Ectopic expression of Fgfr2c in the sutural mesenchyme, without concomitant changes in the expression of FGF ligands, appears to induce the RUNX2-dependent osteogenic program and craniosynostosis in Bcl11b(-/-) mice.
Calvarial osteoblasts from Fgfr2c gain-of-function mice had enhanced osteoblastic function and maturation with concomitant increase in ERK-MAPK activation. In vitro inhibition with U0126 mitigated ERK protein activation levels and reduced alkaline phosphatase activity. FGFR2c-mediated ERK-MAPK signaling is a key mediator of craniofacial growth and coronal suture development.
these data suggest that tropism of influenza Virus to distal lung stem cell niches represents an important factor of pathogenicity and highlight impaired Fgfr2b signaling as underlying mechanism
Fgfr1 and Fgfr2 in the palatal and mandibular mesenchyme have roles in regulating shelf medial wall protrusion and growth of the mandible to coordinate the craniofacial tissue movements that are required for palatal shelf elevation
Data demonstrate an essential role for FGFR1 and FGFR2 in endothelial cells for cardiac functional recovery and vascular remodeling following in vivo cardiac ischemia-reperfusion injury, without affecting the cardiac hypertrophic response.
isolated deletion of Pten failed to stimulate ectopic fiber cell differentiation, and the combined deletion of Pten and Fgfr2 failed to restore differentiation-specific Aquaporin0 and DnaseIIbeta expression in the lens fiber cells
mRNA and protein expression of FGFR-1, FGFR-2 in the porcine umbilical cord during pregnancy.
EGFR, VEGFR and FGFR are expressed in porcine oviduct and endometrium during the time of implantation [review]
analysis of regulation of endometrial fibroblast growth factor 7 (FGF-7) and its receptor FGFR2IIIb
FGFR2 signaling appears to be associated with the regulation of inner cell mass development and proliferation during blastocyst formation in cattle.
activation of FGFR1 and FGFR2 by uterine- and endometrial-derived FGF2 stimulates PI3K/AKT and mitogen-activated protein kinase pathways for development of the porcine uterus and improvement of litter size
it is highly likely that the missense mutation in the FGFR2 gene caused the bovine facial dysplasia syndrome phenotype in a dominant mode of inheritance.
FGF10 and its receptor FGFR2b are more expressed in subordinate follicles; FGF10 acts as an important regulator of follicular growth in cattle.
Alterations in the expression of VEGF-A and bFGF systems suggest that angiogenic factors are involved in abnormal placental development in cloned gestations, contributing to impaired fetal development and poor survival rates.
These data support a role for FGF10 and fibroblast growth factor receptor 2B in signaling to granulosa cells from theca cells and/or the oocyte.(fibroblast growth factor receptor 2B)
FGF10 mRNA expression did not change during functional luteolysis, whereas FGFR2B mRNA abundance decreased significantly at 2, 4, and 12 hr after PGF2alpha, and returned to pretreatment levels for the period 24-64 hr post-PGF2alpha
Fibroblast growth factor receptor 2c signaling is required for intestinal cell differentiation in zebrafish.[Fgfr2c]
we show that minimal amounts of Fgfr1a or Fgfr2 are required to initiate a regulatory cascade in pharyngeal endoderm reducing expression of fsta, thereby allowing correct BMP signaling to the maturing chondrocytes of the head cartilage.
the roles of Fgfr2 signaling in zebrafish left-right asymmetry
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.
fibroblast growth factor receptor 2
, bacteria-expressed kinase
, keratinocyte growth factor receptor
, fibroblast growth factor receptor 2 IIIb
, fibroblast growth factor receptor 2 (bacteria-expressed kinase, keratinocyte growth factor receptor, craniofacial dysostosis 1, Crouzon syndrome, Pfeiffer syndrome, Jackson-Weiss syndrome)
, BEK fibroblast growth factor receptor
, FGF receptor
, hydroxyaryl-protein kinase
, protein tyrosine kinase, receptor like 14
, soluble FGFR4 variant 4
, FGF-7 receptor 2IIIb
, fgf receptor
, chicken tyrosine kinase (cek3)
, receptor tyrosine kinase
, tyrosine kinase receptor CEK3
, fibroblast growth factor receptor-2