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anti-Human FGF10 Antikörper:
anti-Mouse (Murine) FGF10 Antikörper:
anti-Rat (Rattus) FGF10 Antikörper:
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Human Polyclonal FGF10 Primary Antibody für IHC, WB - ABIN6672641
Sun, Cui, Gao, Pan, Zhou, Huang, Lan, Wei, Liu, Liu, Xian: TGF-α Overexpression in Breast Cancer Bone Metastasis and Primary Lesions and TGF-α Enhancement of Expression of Procancer Metastasis Cytokines in Bone Marrow Mesenchymal Stem Cells. in BioMed research international 2018
Fgf3 and Fgf10a work in concert to promote maturation of the epibranchial placodes in zebrafish.
Fgf10 and Fgf3 secreted from the forming neurohypophysis exert direct guidance effects on hypothalamic neurosecretory axons.
through the analysis of fgf10(-/-); fgf24(-/-) embryos, the specific role of these two FGF ligands in the induction of the ventral pancreas and in the repression of the hepatic fate was revealed.
fgf10a, which is expressed in the mesenchyme surrounding non-hepatic endodermal cells, negatively impacts the regulative capacity of endodermal tissues.
Functional investigation of a subset of these genes, fgf10a, tgfb2, pax9, and smad5 revealed their necessity in zebrafish palatogenesis.
Data show that the Ihha-Fgf10 regulatory interaction is realized through a signaling feedback loop between the Ihha-expressing epithelium and Fgf10-expressing mesenchyme.
These data provide in vivo evidence that endodermal cells outside the liver-forming region retain hepatic competence and show that an extrinsic signal, Fgf10a, negatively regulates hepatic competence.
Positional cloning identifies fgf10 as the gene disrupted in daedalus.
Fgf10 signaling from the adjacent mesenchyme is responsible for refining the boundaries
Fgf10 acts redundantly with Fgf24 in the pancreatic lateral plate mesoderm and they are both required to specify the ventral pancreas.
rosettes form cyclically from a progenitor pool at the leading zone of the posterior lateral line primordium as neuromasts are deposited from trailing region; fgf3/10 signals localized to leading zone required for rosette formation & primordium migration
We report the ophthalmological and genetic study of a 19-year-old woman and her relatives suffering from this syndrome. A new probably pathogenic variant is described in the FGF10 gene.
We have revealed significant association of FGFR2 and MAP3K1 polymorphisms with breast cancer.
These results indicated that FGF-2, but not FGF-10, may be supplemented during stem cell expansion to prime cells for successful chondrogenesis and osteogenesis.
The present data indicate that non-natural FGFR2 ligands, such as FGF10 and FGF19, are important factors in the pathophysiology of Aspert syndrome.
data suggest that the strongest signal of association at 5p12 is mediated through coordinated activation of FGF10 and MRPS30, two candidate genes for breast cancer pathogenesis
Fgf10 signaling has an essential role in the formation of lipofibroblasts during late lung development
Expression of Fibroblast Growth Factor 10 is correlated with poor prognosis in gastric adenocarcinoma.
FGF10 has a role in protecting neuron against oxygen-glucose deprivation injury through inducing heme oxygenase-1
Data identify autocrine activation of FGF signaling as an essential mechanism in promoting Pten-deficient skin tumors.
precursor of the hormone Irisin (FNCD5) were abundantly expressed in all three fat depots, along with fibroblast growth factors (FGF) FGF1, FGF7 and FGF10, whereas, FGF19 and FGF21 were undetectable.
The therapeutic potential of the FGF10 treatment.
FGF10 plays an important role for tumor growth by both paracrine and autocrine manner.
The findings show that immunohistochemistry with FGF10, FGFR2b, or SHH could be useful in differentiating CCAM from type I PPB, when a child presents with a focal cystic lung lesion.
Paracrine FGF10 signaling stimulates the differentiation of human stem cell into urothelial cells.
High FGF10 expression is associated with ameloblastoma.
Three FGF10 single nucleotide polymorphisms in complete linkage disequilibrium--rs339501, rs12517396, and rs10462070--were associated with extreme myopia in the Japanese population.
FGF-10 expression during the development of the human hindgut and anorectum suggests that it may play a role in hindgut and anorectal morphogenesis.
The sclera of myopic eyes had higher FGF10 levels. The risk G allele of SNP rs339501 was associated with extreme myopia in human and caused a higher gene expression in the luciferase assay.
the posttranslational and transcriptional mechanisms underlying stimulation of P-glycoprotein function and expression by keratinocyte growth factor-2 (KGF2) that may contribute to the beneficial effects of KGF2 in intestinal inflammatory disorders
tooth agenesis had increased risk of a family history of cancer. tooth agenesis was associated with positive self-reported family history of cancer and variants in FGF10.
Identification of ISL1 transcriptional targets via ChIP-Seq and expression analyses revealed that Isl1 regulates several important signaling pathways during embryonic genital development, including the BMP, WNT, and FGF cascades.
It is concluded that during early pseudoglandular stage of lung development Ptch1 patterns Fgf10 and regulates Foxf1 expression in the lung mesenchyme to direct branch formation and this is essential for proper lobe formation and lung function.
small interfering RNA knockdown of FGFR2 suppressed PI3K/Akt pathway activation by FGF10 and abolished its anti-apoptotic and neurite repair effects in vitro.
the response of FGF10(+) progenitors and differentiated Airway smooth muscle cells to growth factor treatment in real time using lineage tracing in the background of an air-liquid interface (ALI) culture system.
FGF10 pathway is downregulated in Dlx5(-/-) mice, and activation of FGF10 signaling rescues cranial neural crest cell proliferation and myogenic differentiation.
Inactivation of ALX4/Alx4 causes lacrimal gland aplasia in both human and mouse. These results reveal a key role of Alx4 in mediating FGF-Shp2-FGF signaling in the neural crest for lacrimal gland development.
show that during homeostasis, basal stem/progenitor cells in cartilaginous airways maintain their stem cell state by downregulating the Hippo pathway (resulting in increased nuclear Yap), which generates a localized Fgf10-expressing stromal niche
reactivating SHH signaling in mutant lungs rescued the tip dilation phenotype and attenuated FGF signaling. Importantly, the reduced SHH signaling activity did not appear to be caused by decreased Shh expression or protein stability; instead, biologically active form of SHH proteins were reduced in both the Ext1 mutant epithelium and surrounding wild type mesenchymal cells.
that miR-205 in the surface ectoderm functions to ensure robust activation of pathways associated with Fgf10 signaling.
Mesenchymal FGF10 controls the size of the taste bud papillary area, while overall patterning remains unchanged. Results show that FGF signaling negatively affects the extent of canonical Wnt signaling, which is the main activation pathway during fungiform papillae development; however, this effect does not occur at the level of gene transcription.
Sox9 is positively regulated by mesenchymal Fgf10, a process that requires active Erk signaling during salivary gland development
Fgf10 is expressed in the mesenchyme around developing submucosal glands. All nasal glands require FGF10 for branching morphogenesis. FGF10 is required for gland budding and ductal morphogenesis of the Steno's gland and the maxillary sinus glands.
FGFR2c signaling regulates branching morphogenesis through the activation of FGFR2b signaling via increased FGF10 autocrine. These results provide new insight into the mechanisms by which crosstalk between FGFR2b and FGFR2c results in efficient branching morphogenesis.
Decreased Fgf10 mRNA levels lead to congenital lung defects, which are compatible with postnatal survival, but which compromise the ability of the lungs to cope with sub-lethal hyperoxic injury.
Fgf10 enhances the formation of tissue-engineered small intestine.
Lhx9 expression overlapped markedly with FGF10 expression cells in the limb mesenchyme and was associated with proliferative cells of the progress zone.
Hypoplasia of the salivary glands led to a significant reduction in saliva production in Fgf10 heterozygous adult mice
Hoxc8 initiates an ectopic mammary program by regulating Fgf10 and Tbx3 expression and Wnt/beta-catenin signaling
BMP4 promotes activation of FGF7 and FGF10 signaling, leading to an increase in proliferative basal cell population in developing skin.
We conclude that FGF10 and FGFR2B expression is increased in the future subordinate follicle before morphological deviation, which may contribute to follicle selection
We found no difference between treatments regarding embryo production, developmental speed, and gene expression. CONCLUSION: In conclusion, the presence of FGF10 during IVM had no effect on embryo production, developmental speed, and gene expression.
The present data suggest a role for FGF10 in the control of fetal folliculogenesis in cattle.
BMP15 and FGF10 stimulate expansion of in cumulus-oocyte complexes by driving glucose metabolism toward hyaluronic acid production and controlling gene expression in the ovulatory cascade.
Genetic variability is an important component of the number of antral follicles in the bovine ovary.
FGF10 and its receptor FGFR2b are more expressed in subordinate follicles; FGF10 acts as an important regulator of follicular growth in cattle.
These data support a role for FGF10 and fibroblast growth factor receptor 2B in signaling to granulosa cells from theca cells and/or the oocyte.(fibroblast growth factor receptor 2B)
FGF10 mRNA expression did not change during functional luteolysis, whereas FGFR2B mRNA abundance decreased significantly at 2, 4, and 12 hr after PGF2alpha, and returned to pretreatment levels for the period 24-64 hr post-PGF2alpha
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. This protein exhibits mitogenic activity for keratinizing epidermal cells, but essentially no activity for fibroblasts, which is similar to the biological activity of FGF7. Studies of the mouse homolog of suggested that this gene is required for embryonic epidermal morphogenesis including brain development, lung morphogenesis, and initiation of lim bud formation. This gene is also implicated to be a primary factor in the process of wound healing.
, fibroblast growth factor 10
, keratinocyte growth factor 2
, produced by fibroblasts of urinary bladder lamina propria
, obg-like ATPase 1