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FGFR1 and/or FGF3 gene amplification correlated with a lower pathologic complete response in patients with HER2(+) early breast cancer treated with neoadjuvant anti-HER2 therapy
fibroblast growth factor receptor 3 missense mutations were identified in 5 cases of thanatophoric dysplasia
MCF7 cells over-expressing both WNT1 and FGF3 show a 3.5-fold increase in mammosphere formation; conditioned media from these cells also promotes stem cell activity in untransfected parental MCF7 and T47D cells, as WNT1 and FGF3 are secreted factors.
analysis provided evidence for gene-gene interaction between FGF3 (rs4980700) and PAX9 (rs2073242), increasing risk for isolated oral clefts (p = 0.0003). FGF3 is associated with oral clefts and may interact with PAX9.
haplotypes may contribute to the tendon disease process in elite volleyball athletes
FGF3 gene expression is altered in a human breast cancer progression model.
Higher FGF-23 concentration was associated with LVED mass and with incident atrial fibrillation and may, in part, explain the link between chronic kidney disease and AF.
A de novo 290 kb interstitial duplication of chromosome 11q13.3 including the FGF3 and FGF4 genes.
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 FGF3.
This study is the first to show a significant association between coronary calcification and elevated serum FGF 23 in children.
confirm the absence of otodental syndrome in heterozygous FGF3 carriers, but report unilateral microtia in one of them
Manifestations of recessive FGF3 mutations range from fully penetrant LAMM syndrome to deafness with residual inner ear structures and, by extension, with minimal syndromic features.
alterations in dosage of the Fgf3 gene cause dental morphological changes
labyrinth aplasia, microtia, and microdontia (LAMM) syndrome, caused by mutations in FGF3
These findings suggest that the nuclear form of FGF3 inhibits cell proliferation by interfering with ribosomal biogenesis.
Development of the inner ear is completely disturbed at a very early stage--or the otic vesicle is not induced at all--in all of the affected individuals who carried two mutant FGF3 alleles
FGF3, FGF7, FGF10, FGF18, and FGFR1 may have roles in nonsyndromic cleft lip and palate
Implication of FGF3 and FADD in human craniofacial disease.
sequenced the FGF3 gene in 10 unrelated families in which probands had congenital deafness associated with various inner ear anomalies, including Michel aplasia, with or without tooth or external ear anomalies.
study identified a homozygous missense mutation (c.196G-->T) in FGF3 in 21 affected individuals from a large extended family phenotypically characterized by autosomal recessive syndromic congenital sensorineural deafness, microtia and microdontia
results indicate that Fgf3 hypomethylation and gene overexpression, but not protein expression, occurred in the early stage of oral carcinogenesis induced by DBP
We demonstrate that elevated BMP4 depletes PSM progenitors in vitro, phenocopying the Fgf3 mutant, suggesting that excessive BMP signals cause the Fgf3 axis defect. To test this in vivo we increased BMP signaling in Fgf3 mutants by removing one copy of Noggin, which encodes a BMP antagonist.
FGF signaling sustains the odontogenic fate of dental mesenchyme by suppressing beta-catenin signaling.
Ectopic expression of Fgf3 leads to aberrant lineage segregation in the mouse parthenote preimplantation embryos.
Data suggest that Fgf3/Fgfr3 signaling is required for maintenance of Gnrh (gonadotropin-releasing hormone) neurons in aging hypothalamus; postnatal Gnrh system is plastic/resilient, able to override preexisting defects and respond to external cues.
Fgf3 and Fgf10 are not required for specification of cardiovascular progenitors, but rather for their normal developmental coordination.
Microarray analysis was used to identify prospective placode genes that were differently expressed in control and Fgf3(-)(/)(-)embryos.
alterations in dosage of the Fgf3 gene cause dental morphological changes in genetically engineered mutants
Over expression of FGF-3 results in abnormal prostate and Wolffian duct development
transforming capacity of FGF3 attached to phospholipid membrane
inducible expression in mammary gland and mammary gland neoplasms
signalling by FGFR3 plays a more prominent role in cartilage maturation and vascular invasion at the chondro-osseous junction
Fgf-3 transcription is activated by SOX7 and GATA-4, which bind competitively
Fgf3 gene is developmentally regulated by sonic hedgehog (Shh) signalling
Results suggest that Runx2 mediates the functions of epithelial FGF signals regulating Fgf3 expression in the dental mesenchyme and that Fgf3 may be a direct target gene of Runx2.
Data show in mouse that Fgf3 is required during morphogenesis for both auditory and vestibular function.
Disruption in an Fgf3, -10/Dlx5 signaling cascade is operant in molecular mechanisms of inner ear teratogenesis by excess retinoic acid.
Although many reports have pointed to the role of FGF3 in otic regionalisation, we provide evidence that FGF3 is not sufficient to govern this process.
Fgf3 is not required for mouse forebrain development whereas Fgf8 has a central role during this process.
Loss of function of both fgf3 and fgf8a lead to a striking loss of the postchordal neurocranium that can be rescued by restoring Fgf3 and Fgf8a signaling centers in the brain and mesoderm.
Pharmacological inhibition of FGF signaling or a mutation in the fgf3 gene can compensate the gain of caudal hypothalamic dopaminergic neurons in cnot8m1061 mutants, indicating a role for Fgf3 in control of development of this dopaminergic population
Fgf10b participates in a late phase of otic induction and, in combination with fgf3, is especially critical for epibranchial induction.
Fgf3 and Fgf10a work in concert to promote maturation of the epibranchial placodes in zebrafish.
Myogenic factor (Myf)5 modulates craniofacial cartilage development through the fgf3 signaling pathway.
Data indicate that foxi1 is expressed in branchial arch ectoderm and endoderm, and morpholino knock-down of foxi1 causes apoptosis of neural crest in the branchial arches, which is rescued by fgf3.
Fgf10 and Fgf3 secreted from the forming neurohypophysis exert direct guidance effects on hypothalamic neurosecretory axons.
Activation of hs:fgf3 or hs:fgf8 during late blastula/early gastrula stages (5 hpf or earlier) resulted in complete dorsalization of the embryo
In lia(-/-) (fgf3(-/-)) mutants, anterior otic character is reduced, but not lost altogether.
FGF3 and FGF8, is required to establish correct segmental identity throughout the hindbrain and for subsequent neuronal development
Requirement for endoderm and FGF3 in ventral head skeleton formation
Fgf8 and Fgf3 are required for zebrafish ear placode induction, maintenance and inner ear patterning
Data show that compromising Fgf3 and Fgf8 signaling or removing dlx3b, dlx4b and sox9a genes together blocks ear development.
Data show that fibroblast growth factor (Fgf)8 and Fgf3 regulate different aspects of telencephalic development, and that Fgf3 alone is required for the expression of several telencephalic markers.
Fgf3 and Fgf8 as key regulators of cartilage formation in the vertebrate head.
Results show that fibroblast growth factor 3 signaling from the ventral diencephalon is required to induce the expression of lim3, pit1 and other pituitary-specific genes in the underlying adenohypophyseal progenitor cells.
Fgf (3 and 8) signals from rhombomere4, acting through the MapK pathway, then cooperate with Vhnf1 to activate val expression and subsequent rhombomere 5 and rhombomere 6 development
animals doubly reduced for Fgf8 and Fgf3 have severe reductions in hyoid cartilages and the more posterior branchial cartilages
Results suggest that Fgf3 is a major endodermal determinant required for epibranchial placode neurogenesis.
fgf3 can act as otic inducers
Plays an important role in the regulation of embryonic development, cell proliferation, and cell differentiation. Required for normal ear development.
, INT-2 proto-oncogene protein
, V-INT2 murine mammary tumor virus integration site oncogene homolog
, fibroblast growth factor 3 (murine mammary tumor virus integration site (v-int-2) oncogene homolog)
, heparin-binding growth factor 3
, murine mammary tumor virus integration site 2, mouse
, oncogene INT2
, proto-oncogene Int-2
, interacting gene 2
, Int-2 proto-oncogene protein
, Fibroblast growth factor-3