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anti-Human FGF3 Antikörper:
anti-Rat (Rattus) FGF3 Antikörper:
anti-Mouse (Murine) FGF3 Antikörper:
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fibroblast growth factor receptor 3 (zeige FGFR3 Antikörper) missense mutations were identified in 5 cases of thanatophoric dysplasia
MCF7 cells over-expressing both WNT1 (zeige WNT1 Antikörper) 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 (zeige WNT1 Antikörper) and FGF3 are secreted factors.
analysis provided evidence for gene-gene interaction between FGF3 (rs4980700) and PAX9 (zeige PAX9 Antikörper) (rs2073242), increasing risk for isolated oral clefts (p = 0.0003). FGF3 is associated with oral clefts and may interact with PAX9 (zeige PAX9 Antikörper).
FGF3 gene expression is altered in a human breast cancer progression model.
Higher FGF-23 (zeige FGF23 Antikörper) 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 (zeige FGF4 Antikörper) 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 (zeige FGF23 Antikörper) 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 (zeige LAMA2 Antikörper) syndrome to deafness with residual inner ear structures and, by extension, with minimal syndromic features.
results indicate that Fgf3 hypomethylation and gene overexpression, but not protein expression, occurred in the early stage of oral carcinogenesis induced by DBP (zeige GC Antikörper)
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 (zeige CTNNB1 Antikörper) 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 (zeige FGF10 Antikörper) 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
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 (zeige CAD Antikörper) 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 (zeige FGF10 Antikörper) work in concert to promote maturation of the epibranchial placodes in zebrafish.
Myogenic factor (zeige MYOG Antikörper) (Myf)5 (zeige MYF5 Antikörper) modulates craniofacial cartilage development through the fgf3 signaling pathway.
Data indicate that foxi1 (zeige FOXI1 Antikörper) is expressed in branchial arch ectoderm and endoderm, and morpholino knock-down of foxi1 (zeige FOXI1 Antikörper) causes apoptosis of neural crest in the branchial arches, which is rescued by fgf3.
Fgf10 (zeige FGF10 Antikörper) and Fgf3 secreted from the forming neurohypophysis exert direct guidance effects on hypothalamic neurosecretory axons.
In lia(-/-) (fgf3(-/-)) mutants, anterior otic character is reduced, but not lost altogether.
FGF3 and FGF8 (zeige FGF8 Antikörper), 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
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