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anti-Mouse (Murine) FGF8 Antibodies:
anti-Rat (Rattus) FGF8 Antibodies:
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Mouse (Murine) Polyclonal FGF8 Primary Antibody for WB - ABIN1881345
Fleming, Quan, Wang, Amit, Rollins: In vitro characterization of cardiac radiofrequency ablation lesions using optical coherence tomography. in Optics express 2010
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Polyclonal FGF8 Primary Antibody for IHC (p), WB - ABIN540590
Tanaka, Miyamoto, Matsuo, Matsumoto, Yoshida: Human androgen-induced growth factor in prostate and breast cancer cells: its molecular cloning and growth properties. in FEBS letters 1995
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mesenchymal cells of the skull are not fated to form bone, but can be forced into a chondrogenic fate through the manipulation of FGF8 signaling.
We demonstrate with genetic evidence that the Wnt5a gradient acts as a global cue that is instructive in establishing planar cell polarity (PCP) in the limb mesenchyme, and that Wnt5a also plays a permissive role to allow Fgf4 and Fgf8 signaling to orient PCP.
THe Fgf8-Cre reporter expression in isthmic structures in mice include 'signature' isthmic structures in mice include the trochlear nucleus, the dorsal raphe nucleus, the microcellular tegmental nuclei, the pedunculotegmental nucleus, the vermis of the cerebellum, rostral parts of the parabrachial complex and locus coeruleus, and the caudal parts of the substantia nigra and VTA.
Results indicate that perinatal fibroblast growth factor 8 (FGF8) signaling is important for the timing of the onset of anterior-dorsal glial fibrillary acidic protein expression in midline glial cells suggesting that FGF8 function regulates midline GFAP-IR glial cell development, which when disrupted by Fgf8 deficiency prevents the formation of the corpus callosum.
The FBLN1/FGF8 interaction may also be involved in the survival of neural crest cell population during development.
These results indicate that the modulatory effects of SHH on BALB/c mouse metanephric explant cultures may involve the regulation of Fgf8 expression but not Fgf10 expression, which provides evidence for the functional role of Fgf proteins in renal morphogenesis.
FGF-8 was revealed to suppress BMP-induced osteoblast differentiation through the ERK pathway and the effects were enhanced by TNF-alpha.
Fgf8 expression is required for the continued postnatal development/maturation of the Vasopressin and CRH neurons in the Paraventricular nucleus.
Deregulated FGF8 and Otx2/Gbx2 gene expression underlies cerebellar vermis hypoplasia in mouse model of CHARGE syndrome.
Cre fate mapping in Fgf8 mutant embryos revealed novel functions of this gene in rostral patterning center progenitor development. Disruption resulted in aberrant progenitor number and distribution in the rostral telencephalon.
Tfap2a-dependent changes in mouse facial morphology result in clefting that can be ameliorated by a reduction in Fgf8 gene dosage
Results show that DLX5, p63, Pin1 and FGF8 participate to the same time- and location-restricted regulatory loop essential for apical ectodermal ridge stratification, hence for normal patterning and skeletal morphogenesis of the limb buds.
This study demonistrated that Fgf8- and Fgfr1/Fgf8-deficient mice diplay increased anxiety-like behavior and reductions in specific populations of serotonergic neurons in the brain.
Scube3 may be a critical upstream regulator of fast fiber myogenesis by modulating fgf8 signaling during zebrafish embryogenesis
Retinoic acid directly represses Fgf8 through a retinoic acid response element-mediated mechanism that promotes repressive chromatin
Together our data demonstrates that Foxc1 - Fgf8 signaling regulates mammalian jaw patterning and provides a mechanistic basis for the pathogenesis of syngnathia
Data indicate that Foxi3 mutants succumb to apoptosis from embryonic day 9.75 onwards, and this cell death correlates with a delay in expression of Fgf8 in branchial arch ectoderm.
FGF8 is not sufficient to induce ectodermal progenitors of the olfactory pit to acquire neural fate. altered neurogenesis and lack of GnRH neuron specification after reduced Fgf8 expression reflected dysgenesis of the nasal region.
regulation of higher order chromatin organisation during differentiation in the embryo can be uncoupled from the machinery that promotes transcription and, for the first time, identify FGF as an extrinsic signal that can direct chromatin compaction
In Fuz mutants, the phenotype stems from dysregulated Gli processing, which in turn results in excessive craniofacial Fgf8 gene expression.
we employ a sensitive assay of human FGF8 variants in zebrafish to demonstrate that the spectrum of isoforms of FGF8 produced by alternative splicing can provide key insights into the genetic susceptibility to human malformations
results of this study suggest that FGF8 and Survivin contribute to radiation resistance in rectal cancer and may serve as markers to select patients who may not benefit from neoadjuvant radiotherapy
The expression of BMP4 and FGF8 corelates well with the proliferative component of the pathologies, indicating a possible role in the pathogenesis and progression of Odontogenic Cyst and Tumors.
Study demonstrated that FGF8 can regulate germ cell fate by modulating the dynamic equilibrium between differentiation and self-renewal.
FGF8 and FGFR3 may therefore play an important role in the onset of deep zone necrosis and pathogenesis in Kashin-Beck disease in adolescent children.
we also found that FGF8 increased the expression of YAP1 and knockdown of YAP1 eliminated the upregulation of EGFR and the resistance to EGFR inhibition induced by FGF8. Our study provides evidence that FGF8 plays an important role in the resistance to EGFR inhibition of human hepatocellular carcinoma cells
Genetic testing identified a de novo, heterozygous mutation in fibroblast growth factor receptor 1 (FGFR1 p.L630P). L630 resides on the ATP binding cleft of the FGFR1 tyrosine kinase domain, and L630P is predicted to cause a complete loss of receptor function. Cell-based assays confirmed that L630P abolishes FGF8 signaling activity
Bonferroni adjusted p-value: 0.04). No statistically significant associations were identified in the other ethnic groups. In conclusion, variant/s in FGF2 and FGF8 may predispose diabetics with CKD to LEA.
in one holoprosencephaly (HPE) family, a deleterious FGFR1 allele was transmitted from one parent and a loss-of-function allele in FGF8 from the other parent to both affected daughters. This family is one of the clearest examples to date of gene:gene synergistic interactions causing HPE in humans.
Fgf8 activates Ras-ERK pathway to specify hindbrain. Downstream of ERK, Pea3 specifies isthmus (rhombomere 0, r0), and Irx2 may specify r1, where the cerebellum is formed.
Regulation of neurogenesis by Fgf8a requires Cdc42 signaling and a novel Cdc42 effector protein
Our results link FGF8, c-Abl and p300 in a regulatory pathway that controls DeltaNp63alpha protein stability and transcriptional activity.
Data indicate that overexpression of fibroblast growth factor 8 (FGF8) correlates with lymph node metastasis and poor prognosis in colorectal cancer (CRC).
FGF8 mutations (p.Gly29_Arg34dup and p.Pro26Leu) contribute to the formation of the VATER/VACTERL association.
Together, these data demonstrate that FGF (FGFR-2 and Fgf8)signaling regulates cell proliferation and cell polarity and that these cell processes contribute to facial morphogenesis.
The oncoprotein HBXIP enhances angiogenesis and growth of breast cancer through modulating FGF8 and VEGF.
genetic association study in population in Massachusetts: Data suggest that clinical features in Kallmann syndrome (KS) are associated with genetic causes: dental agenesis/digital bony abnormalities are associated with variations/mutations in FGF8.
A novel FGF8b-binding peptide with anti-tumor effect on prostate cancer.
FGF8 and FGF18 signal through divergent pathways in ovarian granulosa cells, despite reportedly similar receptor activation patterns.
Genetic variability is an important component of the number of antral follicles in the bovine ovary.
These results suggest that polymorphisms discovered in DECR1, CBFA2T1, and FGF8 may play a role in the lipid metabolism pathway affecting carcass quality traits in beef cattle.
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 is known to be a factor that supports androgen and anchorage independent growth of mammary tumor cells. Overexpression of this gene has been shown to increase tumor growth and angiogensis. The adult expression of this gene is restricted to testes and ovaries. Temporal and spatial pattern of this gene expression suggests its function as an embryonic epithelial factor. Studies of the mouse and chick homologs revealed roles in midbrain and limb development, organogenesis, embryo gastrulation and left-right axis determination. The alternative splicing of this gene results in four transcript variants.
, androgen-induced growth factor
, heparin-binding growth factor 8
, fibroblast growth factor 8 (androgen-induced)
, fibroblast growth factor 8
, fibroblast growth factor-8
, fibroblast growth factor 8 (androgen-induced) isoform 1
, fibroblast growth factor 8 (androgen-induced) isoform 2
, fibroblast growth factor 8 (androgen-induced) isoform 3