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anti-Human FGFR1 Antibodies:
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Human Polyclonal FGFR1 Primary Antibody for FACS, IF - ABIN1882081
Jiao, Greendorfer, Zhang, Zinn, Diglio, Thompson: Alternatively spliced FGFR-1 isoform signaling differentially modulates endothelial cell responses to peroxynitrite. in Archives of biochemistry and biophysics 2003
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Human Monoclonal FGFR1 Primary Antibody for ELISA, WB - ABIN969138
Hu, Fang, Dunham, Prada, Stachowiak, Stachowiak: 90-kDa ribosomal S6 kinase is a direct target for the nuclear fibroblast growth factor receptor 1 (FGFR1): role in FGFR1 signaling. in The Journal of biological chemistry 2004
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Human Monoclonal FGFR1 Primary Antibody for CyTOF, FACS - ABIN268017
Zhao, Frist, Yeoh, Miller: Modification of alternative messenger RNA splicing of fibroblast growth factor receptors in human cardiac allografts during rejection. in The Journal of clinical investigation 1994
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Human Monoclonal FGFR1 Primary Antibody for CyTOF, FACS - ABIN269474
Sasaki, Ishida, Toyota, Ota, Suzuki, Takaoka, Yasui, Yamamoto, Takagi, Maeda, Seito, Tsujisaki, Shinomura, Imai: Interferon-α/β and anti-fibroblast growth factor receptor 1 monoclonal antibody suppress hepatic cancer cells in vitro and in vivo. in PLoS ONE 2011
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Human Polyclonal FGFR1 Primary Antibody for ELISA, WB - ABIN543048
Fu, Abu-Khalil, Morrison, Geschwind, Kornblum: Expression patterns of epidermal growth factor receptor and fibroblast growth factor receptor 1 mRNA in fetal human brain. in The Journal of comparative neurology 2003
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Human Polyclonal FGFR1 Primary Antibody for IHC (fro), ELISA - ABIN544002
Goriely, McVean, Röjmyr, Ingemarsson, Wilkie: Evidence for selective advantage of pathogenic FGFR2 mutations in the male germ line. in Science (New York, N.Y.) 2003
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Human Polyclonal FGFR1 Primary Antibody for DB - ABIN537618
Sato, Katsumata, Kagami, Hasegawa, Hori, Kawakita, Minowada, Shimotsuka, Shishiba, Yokozawa, Yasuda, Nagasaki, Hasegawa, Hasegawa, Tachibana, Naiki, Horikawa, Tanaka, Ogata: Clinical assessment and mutation analysis of Kallmann syndrome 1 (KAL1) and fibroblast growth factor receptor 1 (FGFR1, or KAL2) in five families and 18 sporadic patients. in The Journal of clinical endocrinology and metabolism 2004
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Human Polyclonal FGFR1 Primary Antibody for ELISA, WB - ABIN543046
Lundin, Rönnstrand, Cross, Hellberg, Lindahl, Claesson-Welsh: Differential tyrosine phosphorylation of fibroblast growth factor (FGF) receptor-1 and receptor proximal signal transduction in response to FGF-2 and heparin. in Experimental cell research 2003
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These results suggest that bFGF activation of neuronal FGFR1 generates filopodial processes in neurons that promote nerve-muscle interaction and facilitate NMJ establishment.
in FGFR1 signalling JNK1 phosphorylation depends on ERK2
Mactosylceramide, an early product in GSL biosynthesis, prevents inappropriate activation of insulin and fibroblast growth factor receptors in Drosophila glial cells and hypertrophy.
Proliferation of epithelial sheath progenitors, the apical cells, was decreased in both htl and ths mutants, while ectopic expression of the Ths ligand led to these cells' over-proliferation suggesting that FGF signaling supports ovarian muscle sheath formation by controlling apical cell number in the developing gonad.
Our data identify FGF signaling through Heartless as a key regulator of astrocyte morphological elaboration in vivo.
identify two transcriptional regulators that function downstream of Heartless signaling in lymph gland progenitors, the ETS protein, Pointed, and the Friend-of-GATA protein, U-shaped, which are required for this Heartless-induced differentiation response
We show that salivary gland posterior migration requires the activities of genes that position the visceral mesoderm precursors, such as heartless, thickveins, and tinman, but does not require a differentiated visceral mesoderm.
identified a region within the N terminus of Dof protein that is required for FGF-dependent signal transduction and is necessary for efficient interaction of Dof with the FGF receptor Heartless
Htl is essential for the differentiation of dorsal mesodermal derivatives
PBL is autonomously required in the mesoderm for cell migration.PBL is required for the ability of HTL to trigger cell shape changes
the signal provided by the CAMs acts via the Heartless fibroblast growth factor receptor (FGFR) as outgrowth is reduced to basal levels in the presence of an FGFR inhibitor or if Heartless function is missing from the neurons.
Data suggest that the longitudinal visceral muscle founder cells (LVMFs) require the function of the Drosophila fibroblast growth factor receptor (FGFR) homolog, Heartless
Activation of Htl signalling produces a less prominent effect on FGF pathway on dorsal muscles than on lateral muscles.Extra founders of dorsal muscles are located in characteristic fashion that is different from that observed for excess lateral founders.
Mesodermal cell spreading is dependent on the FGF receptor Heartless.
Activation of ligand-inducible chimeric FGFR1 (iFGFR1) upregulated TNFAIP3 in an ERK2-dependent manner and TNFAIP3 is required for iFGFR1 activation-promoted ductal carcinoma in situ (DCIS) cell proliferation, tumor growth and progression. Knockout of TNFAIP3 blocks FGFR1 signaling-promoted DCIS cell proliferation suggesting that TNFAIP3 is required for FGFR1 signaling-promoted DCIS growth and progression.
Next generation sequencing of circulating tumor DNA (ctDNA) in 34 patients after progression on CDK4/6 inhibitors identified FGFR1/2 amplification or activating mutations in 14/34 (41%) post-progression specimens.
Gain-of-function mutations in KRAS, FGFR1, and TRPV4 are present in 72% of giant cell lesions of the jaw (GCLJ). TRPV4 mutations induce sustained activation of ERK1/2, indicating that their effects converge with that of KRAS and FGFR1 mutations on the activation of the MAPK pathway in GCLJ.
our findings suggest that increased FGF-2 expression and increased FGFR-1 expression are associated with high-grade oral epithelial dysplasia, and are correlated with the presence of metastasis and adverse outcomes in oral tongue squamous cell carcinoma patients.
Results show that NCAM/FGFR1 signaling appears to be involved in the initial phase of TGF-ss1 initiated epithelial-to-mesenchymal transition which can be effectively suppressed by application of FGFR inhibitor.
findings suggest that ectopically expressed FGFR1 promotes PCa progression, at least in part, by increasing inflammation in the tumor microenvironment
Correlation analysis between FGFR1 gene expression, clinical characteristics, and survival data conducted in an independent cohort of esophageal squamous cell carcinoma patients suggested that FGFR1 gene expression could be an independent prognosis predictive factor as patients with higher FGFR1 had a shorter overall survival.
It has been indicated as a potential molecular target in several types of cancer, including oral squamous cell carcinoma.
PTPRG and FGFR1 interact and colocalize at the plasma membrane where PTPRG directly dephosphorylates activated FGFR1.
our findings reveal that activation of FGFR1 promotes cell proliferation, EMT, and metastasis by the newly defined FGFR1-ERK1/2-SOX2 axis in FGFR1-amplified lung cancer.
S100B may be involved in the FGFR1-mediated inflammatory response during OA, which may be considered as a potential therapeutic target
myeloid/lymphoid neoplasms with FGFR1 rearrangement are a rare entity, with no distinct clinical phenotype. FGFR rearrangement confirmation by FISH should be performed in any hematological malignancy with 8p translocation.
CCND1 , C-MYC , and FGFR1 amplifications were observed in 34.28%, 28.57%, and 17.14% of the 35 samples (invasive ductal breast carcinoma).
High FGFR1 expression is associated with Peritoneal Dissemination Via Epithelial-to-Mesenchymal Transition in Gastric Cancer.
The present study aimed to evaluate the relationship between a common FGFR1 single nucleotide polymorphism (rs13317) with craniofacial morphology.
Clinical outcomes of myeloid/lymphoid neoplasms with fibroblast growth factor receptor-1 (FGFR1) rearrangement
Suggest that genomic alterations involving the cell cycle (TP53, CCND1, CDKN2A), as well as FGFR1 amplifications and tumour genomic alterations burden are prognostic biomarkers of survival in head and neck squamous cell carcinoma.
novel heterozygous frameshift mutation c.299_300insCCGCAGACTCCGGCCTCTATGC (p.C101Rfs*17) associated with Kallmann syndrome
FGFR3, as well as its downstream regulatory PI3K/AKT kinases, may serve as potential biomarkers for the invasiveness and prognosis of laryngeal cancer.
Our experiments presented a new mechanism adopted by GDNF supporting glioma development and indicated a possible therapeutic potential via the inhibition of proN-cadherin/FGFR1 interaction.
Results suggest that while the trophectoderm (TE) development is specified in fibroblast growth factor receptor 1 (Fgfr1) mutants, its differentiation abilities are compromised leading to defects at implantation.
FGFR1 and FGFR2 regulate FGFRL1 expression.
Deletion of Fgfr1 in Temporomandibular joint chondrocytes delayed Temporomandibular joint Temporomandibular joint osteoarthritis progression in the age-associated spontaneous Temporomandibular joint osteoarthritis model and the abnormal dental occlusion Temporomandibular joint osteoarthritis model.
a modified ciliary transport pathway used for Pcdh15 transport into the cilium of the inner ear hair cell and coordinated by FGFR1 activity.
Oligodendroglial FGFR1 deficient mice (-/-) showed a significantly ameliorated disease course in MOG35-55 -induced experimental autoimmune encephalomyelitis. Less myelin and axonal loss, and reduced lymphocyte and macrophage/microglia infiltration were found in Fgfr1(-/-) mice. Reduction in disease severity in Fgfr1(ind-/-) mice was accompanied by ERK/AKT phosphorylation, and increased expression of BDNF and TrkB.
Suboptimal FGFR activation by a weak FGF1-FGFR dimer is sufficient to evoke a metabolic response, whereas full FGFR activation by stable and sustained dimerization is required to elicit a mitogenic response.
the close proximity between AcSDKP and FGFR1 was essential for the suppression of TGFbeta/smad signaling and EndMT associated with MAP4K4 phosphorylation (P-MAP4K4) in endothelial cells.
FGFR1 is a driver oncogene in de novo, FGFR1-overexpressing acute myeloid leukemia
Visceral adipose tissue-derived factors stimulate cell transformation through FGFR-1.
the localization of FGF9 and its receptors at different embryonic and postnatal stages in mice testes, was examined.
CDC42 is involved in the trafficking of FGF receptors to the cell membrane to regulate epicardium formation.
MAPK cascades participate in osteogenesis, but only the ERK signaling pathway responds to FGFR1.
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.
clearly demonstrate the different specificity of FGF12-FGFR1c2 and FGF22-FGFR1c2 for well defined HS structures and suggest that it is now possible to chemoenzymatically synthesize precise HS polysaccharides that can selectively mediate growth factor signaling
The study supports a pro-adipogenic role for betaKlotho in skeletal muscle fibro/adipogenesis and calls for further research on involvement of the FGF-FGFR-betaKlotho axis in the fibro/adipogenic infiltration associated with functional deterioration of skeletal muscle in aging and muscular dystrophy.
These new findings reveal that the FGF21-betaKlotho-FGFR1 signaling axis plays roles in maintaining phospholipid homeostasis and the dynamic functions of the lipid droplet, whereas protecting against ER stress, and suggest a potential link of phospholipid biosynthesis, lipid droplet dynamics, ER stress, and energy homeostasis in adipose tissue coordinated by this signaling axis.
Data suggest that Fgf1-mediated signaling represents an important signaling cascade related to adipogenesis and visceral adiposity; expression of Fgf1 (fibroblast growth factor 1) and Fgfr1 (fibroblast growth factor receptor 1) is up-regulated in adipose tissue of obese mice (both obese mice due to high-fat diet and obese mice due to genetic deletion of leptin).
FGFR1OP2-FGFR1 fusion in hematopoietic stem cells induced myeloid leukemia and T-cell lymphoma in a mouse model.
MiR-214 was up-regulated in mesenchymal stem cells of osteoporotic mice and down-regulated during osteoblast differentiation of mesenchymal stem cells. FGFR1 is a direct target of miR-214.
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
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.
Heparan sulfate glycosaminoglycans affect FGF signalling by interacting with both the growth factor and the receptor
mRNA and protein expression of FGFR-1, FGFR-2 in the porcine umbilical cord during pregnancy.
High expression of VEGF-A/VEGFR-2 and FGF-2/FGFR-1 but not of PDGF-BB/PDGFR-beta may contribute to immature and inflammatory intraplaque angiogenesis and plaque instability in a rabbit model of atherosclerosis.
Here we demonstrate that of the nine FGFR1 mutations recently detected in our screen of over 200 HPE probands by next generation sequencing, only five distinct mutations in the kinase domain behave as dominant-negative mutations in zebrafish over-expression assays
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.
Considering all these findings, we concluded that as in mammals, in adult zebrafish the metabolism of lipid and bile acids in the liver are regulated by Fgf signaling.
Data indicate that fgf20a, fgf24, FGF receptor fgfr1 are expressed in normal and regenerating barbel tissue.
Shroom3 is required downstream of FGF signalling to mediate proneuromast assembly in zebrafish.
Requirement of Fgf signaling to maintain photoreceptors and for proliferation during regeneration in the adult zebrafish retina.
Mutation of the gene encoding Fgfr1a simultaneously increases aggression, boldness, and exploration in adult zebrafish.
fgfr expression is directly or indirectly regulated by FGF signaling during epiboly and at the end of somitogenesis.
we describe cloning and expression analysis of the zebrafish fibroblast growth factor receptor 1 ( fgfr1).
knock-down of Fgfr1, but not muscle segment homeobox B, affected the blastemal expression of msxc, suggesting this technique can be used to determine epistasis in genetic pathways affecting regeneration
Bmp and Fgf signaling are essential for liver specification in zebrafish.
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 (FGFR) 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 binds both acidic and basic fibroblast growth factors and is involved in limb induction. Mutations in this gene have been associated with Pfeiffer syndrome, Jackson-Weiss syndrome, Antley-Bixler syndrome, osteoglophonic dysplasia, and autosomal dominant Kallmann syndrome 2. Chromosomal aberrations involving this gene are associated with stem cell myeloproliferative disorder and stem cell leukemia lymphoma syndrome. Alternatively spliced variants which encode different protein isoforms have been described\; however, not all variants have been fully characterized.
fibroblast growth factor receptor
, fibroblast growth factor receptor-1
, basic fibroblast growth factor receptor 1
, FGF receptor
, fibroblast growth factor receptor 1
, fibroblast growth factor receptor 1 (fms-related tyrosine kinase 2, Pfeiffer syndrome)
, ibroblast growth factor receptor 1 (fms-related tyrosine kinase 2, Pfeiffer syndrome)
, basic fibroblast growth factor receptor 1-like
, FGFR1/PLAG1 fusion
, FMS-like tyrosine kinase 2
, fms-related tyrosine kinase 2
, heparin-binding growth factor receptor
, hydroxyaryl-protein kinase
, proto-oncogene c-Fgr
, FGF receptor-1
, cek1 protein
, tyrosine kinase receptor CEK1
, basic fibroblast growth factor receptor 1-A
, fibroblast growth factor receptor 1-A