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Human FGF18 ELISA Kit for Sandwich ELISA - ABIN418594
Koneczny, Schulenburg, Hudec, Knöfler, Holzmann, Piazza, Reynolds, Valent, Marian: Autocrine fibroblast growth factor 18 signaling mediates Wnt-dependent stimulation of CD44-positive human colorectal adenoma cells. in Molecular carcinogenesis 2015
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 (show FGF1 ELISA Kits), and FGF2 (show FGF2 ELISA Kits).
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 (show TIMP1 ELISA Kits) expression.
Tumors from ovarian cancer patients had increased FGF18 expression levels with microvessel density and M2 macrophage infiltration.
FGF8 (show FGF8 ELISA Kits), FGF17 (show FGF17 ELISA Kits), and FGF18 are involved in autocrine and paracrine signaling in HCC (show FAM126A ELISA Kits) 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 (show FGF2 ELISA Kits) and -18 bind to discrete structures on the heparan sulfate chains attached to chondrocyte-derived perlecan (show HSPG2 ELISA Kits) which modulate the growth factor activities
Elevation of FGF signaling, mainly due to increased Fgf18 expression upon inactivation of Evc2 (show EVC2 ELISA Kits) 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 (show EVC2 ELISA Kits) mutant mice
Loss of alleles of Fgf9 and Fgf18 also affect the expression of genes encoding other key intrinsic skeletal regulators, including IHH (show IHH ELISA Kits), PTHLH (PTHrP (show PTHLH ELISA Kits)), and RUNX2 (show RUNX2 ELISA Kits), 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 (show ELN ELISA Kits) synthesis by induction of VEGF-A (show VEGFA ELISA Kits) and fibroblast growth factor (FGF)-18, respectively
novel Shh (show SHH ELISA Kits)-Foxf (show FOXF1 ELISA Kits)-Fgf18-Shh (show SHH ELISA Kits) circuit in the palate development molecular network, in which Foxf1 (show FOXF1 ELISA Kits) and Foxf2 (show FOXF2 ELISA Kits) regulate palatal shelf growth downstream of Shh (show SHH ELISA Kits) signaling, at least in part, by repressing Fgf18 expression
post-natal induction of chondrocyte autophagy is mediated by the growth factor FGF18 through FGFR4 (show FGFR4 ELISA Kits) and JNK (show MAPK8 ELISA Kits)-dependent activation of the autophagy initiation complex VPS34 (show PIK3C3 ELISA Kits)-beclin-1 (show BECN1 ELISA Kits)
Phlpp1 (show PHLPP1 ELISA Kits) deficiency increases Akt2 (show AKT2 ELISA Kits) activity, which diminishes FoxO1 (show FOXO1 ELISA Kits) levels and induces Fgf18 expression to stimulate chondrocyte proliferation.
These results suggest that FGF18 accelerates osteogenesis by upregulation of Bmp2 (show BMP2 ELISA Kits) as well as maintenance or upregulation of Fgfr1 (show FGFR1 ELISA Kits), -2 and -3 expression in osteoblasts.
Fgf-10 (show FGF10 ELISA Kits) and Fgf-18 are expressed specifically within ventral tanycyte subpopulations.
Foxp1 (show FOXP1 ELISA Kits) 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.
FGF18 is proapoptotic in vivo and may act through a mechanism involving the BBC3 (show BBC3 ELISA Kits)-MDM2 (show MDM2 ELISA Kits) pathway.
FGF8 (show FGF8 ELISA Kits) 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