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EGR1 is a major upstream component of FGF signaling in theca cells and that it directs cell fate toward proliferation.
In primary gastric cancer samples, FGF18 was overexpressed in genomically stable and chromosomal instability subtypes of GC. Overexpression was associated with poor survival. FGF18 knockdown inhibited tumor formation abilities, induced G1 phase cell cycle arrest, enhanced anti-cancer drug sensitivity, activated ATM pathway but quenched TGF-beta pathway. FGF18 was a direct target of tumor suppressor, miR-590-5p.
High FGF18 expression is associated with angiogenesis in hepatocellular carcinoma.
FGF18 played an important role in the growth and metastasis of breast cancer.
we genotyped rs9313548 and performed case-control-based association analysis with developmental dyslexia in a Chinese population. Our results were in consistent with previous studies as we did not observe significant association of rs9313548 with developmental dyslexia.
the suppressive effect of miR-139 on FGF18 and in turn on proliferation, apoptosis, invasion, migration and tumor-induced angiogenesis of HCC cells was investigated. FGF18 was suggested as a prognostic biomarker and therapeutic target in HCC patients and miR-139 may be a promising strategy used in HCC treatment via the suppression of FGF18
the results suggest that FGF18 may be involved in MC3T3E1 cell proliferation and osteoblastic differentiation.
significantly increased in endometrioid adenocarinoma
FGF9 and FGF18 increased the migratory capacities of human lung fibroblasts, and FGF9 actively modulated matrix metalloproteinase activity in idiopathic pulmonary fibrosis.
FGF18 serves an essential role in the growth and migration of non-small cell lung cancer cells by regulating the ERK, p38 signaling pathways and MMP26 protein levels.
Data suggest that the combination of FIGO stage, ovarian carcinoma type, and/or fibroblast growth factor 18 (FGF18) score could predict poor prognosis among ovarian carcinoma patients.
The position of sulfate ions bound to FGF18 provides insight into the putative HS-binding site and allows comparison with the prototypical FGFs, FGF1, and FGF2.
role for FGF-18 in chondrogenic and osteogenic events which drive discal development and ossification of the vertebral bodies.
Fgf18 as a molecule that protects articular cartilage by gene expression profiling, and the anticatabolic effects may at least partially be mediated by the Timp1 expression.
Tumors from ovarian cancer patients had increased FGF18 expression levels with microvessel density and M2 macrophage infiltration.
FGF8, FGF17, and FGF18 are involved in autocrine and paracrine signaling in HCC and enhance the survival of tumor cells under stress conditions, malignant behavior, and neoangiogenesis.
There was an association between gene FGF18 rs4043716 and nonsyndromic cleft lip with or without palate in Chinese population.
FGF2 and -18 bind to discrete structures on the heparan sulfate chains attached to chondrocyte-derived perlecan which modulate the growth factor activities
fibroblast growth factor 18 seems to play a role in maintenance of chondrocyte properties, although its expression was rather high in dedifferentiated chondrocytes.
mRNA expression examined by in situ hybridization in whole human embryos at 30 days and 8 weeks of gestation.
Study found that Fgf18 mRNA was one of the spinal motor neurons (SMNs)-specific FGFs in adult mice. Fgf18 mRNA was expressed in the spinal cord, and to a lesser extent in the diaphragm, in mouse embryos. In C2C12 myotubes, FGF18 enhanced AChR clustering. These data propose that FGF18 plays a pivotal role in AChR clustering and NMJ formation in mouse embryogenesis.
Elevation of FGF signaling, mainly due to increased Fgf18 expression upon inactivation of Evc2 in the perichondrium, critically contributes to the pathogenesis of limb dwarfism. The limb dwarfism phenotype is partially rescued by inactivation of one allele of Fgf18 in the Evc2 mutant mice
Loss of alleles of Fgf9 and Fgf18 also affect the expression of genes encoding other key intrinsic skeletal regulators, including IHH, PTHLH (PTHrP), and RUNX2, revealing potential direct, indirect, and compensatory mechanisms to coordinate chondrogenesis and osteogenesis.
retinoic acid is produced by pulmonary endothelial cells and regulates pulmonary angiogenesis and elastin synthesis by induction of VEGF-A and fibroblast growth factor (FGF)-18, respectively
novel Shh-Foxf-Fgf18-Shh circuit in the palate development molecular network, in which Foxf1 and Foxf2 regulate palatal shelf growth downstream of Shh signaling, at least in part, by repressing Fgf18 expression
post-natal induction of chondrocyte autophagy is mediated by the growth factor FGF18 through FGFR4 and JNK-dependent activation of the autophagy initiation complex VPS34-beclin-1
Phlpp1 deficiency increases Akt2 activity, which diminishes FoxO1 levels and induces Fgf18 expression to stimulate chondrocyte proliferation.
These results suggest that FGF18 accelerates osteogenesis by upregulation of Bmp2 as well as maintenance or upregulation of Fgfr1, -2 and -3 expression in osteoblasts.
Fgf-10 and Fgf-18 are expressed specifically within ventral tanycyte subpopulations.
Foxp1 regulates the quiescent stem cell state in the hair follicle stem cell niche by controlling Fgf18 expression.
These findings therefore argue for an involvement of FGF18 in the control of various developmental events during the alveolar stage.
Fgf-18 is an important mediator of bone regeneration, which is required during later stages of bone regeneration.
FGF18 is upregulated during osteoblast differentiation induced by dexamethasone in murine mesenchymal stem cells.
Regulation of Hmgn1 and Fgf18 at the digit-interdigit junction suggests retinoic acid controls tissue remodeling as well as apoptosis.
Data revealed interaction between Glg1 and Fgf18 both genetically and physically and reveals a novel regulatory mechanism for Fgf18 signaling involving Glg1 and Dlk.
The expression from early streak stage to midgestation of Fgf18 is measured. It is, closely related to Fgf8 (56.8% identical at the amino acid level). Fgf18 RNA is not expressed until later, in paraxial mesoderm.
FGF-18 may therefore compensate for the action of FGF-2 on bone and cartilage.
expression of FGF18 in calvarial and limb development
Fibroblast growth factor 18 influences proximal programming during lung morphogenesis
Coordination of chondrogenesis and osteogenesis by fibroblast growth factor 18
FGF18 is proapoptotic in vivo and may act through a mechanism involving the BBC3-MDM2 pathway.
FGF8 and FGF18 signal through divergent pathways in ovarian granulosa cells, despite reportedly similar receptor activation patterns.
these data point to a unique role for FGF18 in signaling from theca cells to granulosa cells and suggest that FGF18 influences the process of atresia in ovarian follicles.
The protein encoded by this gene is a member of the fibroblast growth factor (FGF) family. FGF family members possess broad mitogenic and cell survival activities, and are involved in a variety of biological processes, including embryonic development, cell growth, morphogenesis, tissue repair, tumor growth, and invasion. It has been shown in vitro that this protein is able to induce neurite outgrowth in PC12 cells. Studies of the similar proteins in mouse and chick suggested that this protein is a pleiotropic growth factor that stimulates proliferation in a number of tissues, most notably the liver and small intestine. Knockout studies of the similar gene in mice implied the role of this protein in regulating proliferation and differentiation of midline cerebellar structures.
, fibroblast growth factor 18
, fibroblast growth factor 18, like
, fibroblast growth factor 18b