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the suppressive effect of miR (zeige MLXIP Antikörper)-139 on FGF18 and in turn on proliferation, apoptosis, invasion, migration and tumor-induced angiogenesis of HCC (zeige FAM126A Antikörper) cells was investigated. FGF18 was suggested as a prognostic biomarker and therapeutic target in HCC (zeige FAM126A Antikörper) patients and miR (zeige MLXIP Antikörper)-139 may be a promising strategy used in HCC (zeige FAM126A Antikörper) treatment via the suppression of FGF18
the results suggest that FGF18 may be involved in MC3T3E1 cell proliferation and osteoblastic differentiation.
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 (zeige EPHB2 Antikörper), p38 (zeige CRK Antikörper) signaling pathways and MMP26 (zeige MMP26 Antikörper) 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 (zeige FGF1 Antikörper), and FGF2 (zeige FGF2 Antikörper).
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 (zeige TIMP1 Antikörper) expression.
Tumors from ovarian cancer patients had increased FGF18 expression levels with microvessel density and M2 macrophage infiltration.
FGF8 (zeige FGF8 Antikörper), FGF17 (zeige FGF17 Antikörper), and FGF18 are involved in autocrine and paracrine signaling in HCC (zeige FAM126A Antikörper) and enhance the survival of tumor cells under stress conditions, malignant behavior, and neoangiogenesis.
Elevation of FGF signaling, mainly due to increased Fgf18 expression upon inactivation of Evc2 (zeige EVC2 Antikörper) 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 (zeige EVC2 Antikörper) 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 (zeige ELN Antikörper) synthesis by induction of VEGF-A (zeige VEGFA Antikörper) and fibroblast growth factor (FGF)-18, respectively
novel Shh (zeige SHH Antikörper)-Foxf (zeige FOXF1 Antikörper)-Fgf18-Shh (zeige SHH Antikörper) circuit in the palate development molecular network, in which Foxf1 (zeige FOXF1 Antikörper) and Foxf2 (zeige FOXF2 Antikörper) regulate palatal shelf growth downstream of Shh (zeige SHH Antikörper) signaling, at least in part, by repressing Fgf18 expression
post-natal induction of chondrocyte autophagy is mediated by the growth factor FGF18 through FGFR4 (zeige FGFR4 Antikörper) and JNK (zeige MAPK8 Antikörper)-dependent activation of the autophagy initiation complex VPS34 (zeige PIK3C3 Antikörper)-beclin-1 (zeige BECN1 Antikörper)
Phlpp1 (zeige PHLPP1 Antikörper) deficiency increases Akt2 (zeige AKT2 Antikörper) activity, which diminishes FoxO1 (zeige FOXO1 Antikörper) levels and induces Fgf18 expression to stimulate chondrocyte proliferation.
These results suggest that FGF18 accelerates osteogenesis by upregulation of Bmp2 (zeige BMP2 Antikörper) as well as maintenance or upregulation of Fgfr1 (zeige FGFR1 Antikörper), -2 and -3 expression in osteoblasts.
Fgf-10 (zeige FGF10 Antikörper) and Fgf-18 are expressed specifically within ventral tanycyte subpopulations.
Foxp1 (zeige FOXP1 Antikörper) 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 (zeige BBC3 Antikörper)-MDM2 (zeige MDM2 Antikörper) pathway.
FGF8 (zeige FGF8 Antikörper) 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