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anti-Human FGFR4 Antikörper:
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Human Polyclonal FGFR4 Primary Antibody für IHC (p), ELISA - ABIN544004
Yu, Asa, Weigel, Ezzat: Pituitary tumor AP-2alpha recognizes a cryptic promoter in intron 4 of fibroblast growth factor receptor 4. in The Journal of biological chemistry 2003
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Human Monoclonal FGFR4 Primary Antibody für IHC, ELISA - ABIN969139
Ezzat, Zheng, Winer, Asa: Targeting N-cadherin through fibroblast growth factor receptor-4: distinct pathogenetic and therapeutic implications. in Molecular endocrinology (Baltimore, Md.) 2006
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Human Monoclonal FGFR4 Primary Antibody für ICC, ELISA - ABIN969140
Streit, Mestel, Schmidt, Ullrich, Berking: FGFR4 Arg388 allele correlates with tumour thickness and FGFR4 protein expression with survival of melanoma patients. in British journal of cancer 2006
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Human Monoclonal FGFR4 Primary Antibody für IHC, ELISA - ABIN966140
Angelin: Telling the liver (not) to make bile acids: a new voice from the gut? in Cell metabolism 2005
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Human Monoclonal FGFR4 Primary Antibody für IF, ELISA - ABIN966141
Huang, Yang, Luo, Jin, Wang, McKeehan: FGFR4 prevents hyperlipidemia and insulin resistance but underlies high-fat diet induced fatty liver. in Diabetes 2007
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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.
FGF19 gene amplification corresponds with an increased dependency upon FGF19/FGFR4 autocrine signaling in HNSCC.
The results of this study show that FGFR4 Single Nucleotide Polymorphism rs351855 is associated with up-regulation of FGFR4 protein expression and a worse prognosis in breast cancer.
we identified forkhead box C1 (FOXC1) as a novel regulator of colorectal cancer metastases. FOXC1 directly binds its target genes integrin alpha7 (ITGA7) and fibroblast growth factor receptor 4 (FGFR4) and activates their expression
The expression of FGFR4 in the cervical cancer and cervical intraepithelial neoplasia tissues was correlated with the HPV infection and the FGFR4 may be involved in the development of the HPV-infected cervical lesions
The FGFR4-388arg variant promotes lung cancer progression by N-cadherin induction.
These findings suggest that high levels of FGFR4 can increase glucose metabolism and lead to chemoresistance in breast cancer and reveal the mechanistic basis for targeting FGFR4 as a therapeutic opportunity for chemoresistant tumors.
Taken together, this study provides the first evidence that Blu9931 functions as a FGFR4-selective inhibitor in colorectal cancer (CRC) cells, and Blu9931 may be a new targeted drug.
Results show that FGFR4 promotes gastric cancer cell proliferation, migration and epithelial-to-mesenchymal transition. Its expression is negatively regulated by miR-491-5p through SNAIL protein.
Our findings indicate that the FGFR4-388Arg variant may play an important role in lung squamous cell carcinoma, which may be mediated by the overactivation of the MAPK pathway.
FGFR4 rs351855 could be a novel independent prognostic factor of BCR after radical prostatectomy in the Chinese population.
This meta-analysis demonstrates the FGFR rs351855 G>A polymorphism is associated with increased cancer risk.
Our results indicate that mRNA expression of FGFR4-related genes may be a biomarker to define the distinctive molecular phenotype of intrahepatic cholangiocarcinoma
The present study employed FGFR4 polymorphism to help identify treatments for high risk patients with stage III colon cancer.
Our data indicate that FGFR4 polymorphic isoforms mediate signaling that yields mitochondrial therapeutic targets of relevance to the actions of different somatostatin analogs.
In radiosensitive SW480 and DLD1 cells, enforced expression of FGFR4 stabilized RAD51 protein levels resulting in enhanced clearance of gamma-H2AX foci and increased cell survival in the mismatch repair (MMR)-proficient SW480 cells.
FGFR4/FGF19 autocrine signaling mediates the survival of a subset of basal-like breast cancer cells
Study shows that loss of FGFR4 expression led to a remarkable increase in sorafenib-induced ROS generation and apoptosis of hepatocellular carcinoma (HCC) cell lines, and demonstrates that hyperactivation of FGF19/FGFR4 signaling in HCC is one of the main mechanisms of sorafenib resistance.
This is the first study to elucidate FGF19/FGFR4 signaling in favor of hepatocellular carcinoma cells developing from fatty liver
High expression of FGFR4 is associated with hepatocellular carcinoma.
Findings show that FGF19 provides a cytoprotective role against ER stress by activating a FGFR4-GSK3beta-Nrf2 signaling cascade, suggesting targeting this signaling node as a candidate therapeutic regimen for hepatocellular carcinoma (HCC) management.
our data highlight a role of FGF23/FGFR4 signaling in the regulation of cardiac remodeling and function, and indicate that pharmacological interference with cardiac FGF23/FGFR4 signaling might protect from CKD- and age-related LVH.
ileal FGF15/19 to hepatic FGFR4 axis is activated and promotes liver regeneration (LR) after partial hepatectomy (PH) in mice, supporting the potential of ileal FGF15/19 to hepatic FGFR4 axis-targeted therapy to enhance LR after PH
FRS2alpha-mediated pathways are essential for the FGF15/FGF19-FGFR4 signaling axis to control bile acid homeostasis.
Results indicate that FGFR4 is an important growth signal receptor in gastric cancer cells with high FGFR4 expression.
The findings suggest that the primary role of Fgfr3 and Fgfr4 is to control the orderly formation of elastin fibers. In a normal lung, FGFR3 and FGFR4 restrict the expression of MFAP5, among other elastogenesis factors.
FGF23 augments pro-fibrotic signalling cascades in injury-primed renal fibroblasts via activation of FGFR4
the localization of FGF9 and its receptors at different embryonic and postnatal stages in mice testes, was examined.
Blocking FGFR4 inhibits cardiac calcineurin/NFAT signaling and attenuates the development of LVH and cardiac fibrosis in a well-established animal model of CKD without significantly altering kidney function, blood pressure, or FGF23 levels.
The FGFR4 transmembrane polymorphic variants can modulate cellular growth and sensitivity to glucocorticoid hormone negative feedback.
FGFR4 deficiency in mice leads to improvement in glucose metabolism, insulin sensitivity, and reduction in body weight under high fat conditions.
The FGFR4-R388 allele yields a receptor variant that preferentially promotes STAT3/5 signaling.
study shows FGFR4 is specifically up regulated by PAX3-FOXO1; however this FGFR4 over expression does not contribute to PAX3-FOXO1 tumorigenic phenotypes in primary skeletal muscle myoblasts
findings suggest a modulatory role for FGFR4 in the development and progression of hepatocellular carcinoma and that FGFR4 may be an important and novel therapeutic target in treating this disease
Differential specificity of endocrine FGF19 and FGF21 to FGFR1 and FGFR4 in complex with KLB.
FGFR3 and 4 are the receptors that regulate serum 1,25(OH)(2)Vitamin D(3) levels in response to FGF23.
FGFR4 activation mediates the induction of hepatocyte proliferation and the suppression of bile acid biosynthesis by FGF19.
These studies suggest that FGFR1, FGFR3, and FGFR4 act in concert to mediate FGF23 effects on the kidney and that loss of FGFR function leads to feedback stimulation of Fgf23 expression in bone
Fibroblast growth factor receptor-4 Gly388Arg polymorphism is associated with gastric cancer progression
Metabolic regulator betaKlotho interacts with fibroblast growth factor receptor 4 (FGFR4) to induce apoptosis and inhibit tumor cell proliferation.
Fgfr4 mediates a signal-transduction pathway between Wnt16 and Dlc, but not Dld, to regulate haematopoietic stem cells specification.
The analysis of receptor-ligand interactions between D. rerio fgf8 and its receptors, fgfr1 and fgfr4, using combined spectroscopy methods are reported.
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 would consist 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. The genomic organization of this gene, compared to members 1-3, encompasses 18 exons rather than 19 or 20. Although alternative splicing has been observed, there is no evidence that the C-terminal half of the IgIII domain of this protein varies between three alternate forms, as indicated for members 1-3. This particular family member preferentially binds acidic fibroblast growth factor and, although its specific function is unknown, it is overexpressed in gynecological tumor samples, suggesting a role in breast and ovarian tumorigenesis.
fibroblast growth factor receptor 4
, FGF receptor 4
, hydroxyaryl-protein kinase
, protein-tyrosine kinase
, tyrosine kinase related to fibroblast growth factor receptor
, tyrosylprotein kinase
, CTLA-2-beta protein
, fibroblast growth factor receptor 4 16 minus form
, protein-tyrosine kinase receptor MPK-11
, fibroblast growth factor receptor FREK
, fibroblast growth factor receptor-like embryonic kinase
, fibroblast growth factor receptor 4c