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Fibroblast growth factor 16

FGF16, Fibroblast growth factor-16
fibroblast growth factor; may play a role in the development of brown adipose tissue [RGD, Feb 2006] (from NCBI)
Top mentioned proteins: Fibroblast Growth Factor 2, Fibroblast Growth Factor 10, ACID, int-2, FGF18
Papers on FGF16
Instability restricts signaling of multiple fibroblast growth factors.
Krejci et al., Brno, Czech Republic. In Cell Mol Life Sci, Jun 2015
We report that FGF1, FGF3, FGF4, FGF6, FGF8, FGF9, FGF10, FGF16, FGF17, FGF18, FGF20, and FGF22 exist as unstable proteins, which are rapidly degraded in cell cultivation media.
Genetic mechanisms leading to primary amenorrhea in balanced X-autosome translocations.
Melaragno et al., São Paulo, Brazil. In Fertil Steril, May 2015
The ZDHHC15 gene belongs to a conserved syntenic region that encompasses the FGF16 gene, which plays a role in female germ line development.
Heart-specific expression of FGF-16 and a potential role in postnatal cardioprotection.
Cattini et al., Canada. In Cytokine Growth Factor Rev, Feb 2015
Fibroblast growth factor 16 (FGF-16) was originally cloned from rat heart.
HaloTag is an effective expression and solubilisation fusion partner for a range of fibroblast growth factors.
Fernig et al., Luxembourg, Luxembourg. In Peerj, 2014
Moreover, whereas FGF6, FGF8, FGF16, FGF17, FGF20 and FGF22 were only expressed as insoluble proteins, their N-terminal HaloTag fusion counterparts (Halo-FGFs) were soluble, and could be successfully purified.
Identification of three novel FGF16 mutations in X-linked recessive fusion of the fourth and fifth metacarpals and possible correlation with heart disease.
Nordgren et al., Stockholm, Sweden. In Mol Genet Genomic Med, 2014
Nonsense mutations in FGF16 have recently been linked to X-linked recessive hand malformations with fusion between the fourth and the fifth metacarpals and hypoplasia of the fifth digit (MF4; MIM#309630).
Further evidence for FGF16 truncating mutations as the cause of X-linked recessive fusion of metacarpals 4 / 5.
Mundlos et al., Poznań, Poland. In Birth Defects Res A Clin Mol Teratol, 2014
Recently, we have identified FGF16 nonsense mutations as the underlying cause of isolated X-linked recessive MF4.
Chromosome X-wide association study identifies Loci for fasting insulin and height and evidence for incomplete dosage compensation.
Ripatti et al., Helsinki, Finland. In Plos Genet, 2014
In a chrX-wide association analysis, we identify three novel loci: two for height (rs182838724 near FGF16/ATRX/MAGT1, joint P-value = 2.71×10(-9), and rs1751138 near ITM2A, P-value = 3.03×10(-10)) and one for fasting insulin (rs139163435 in Xq23, P-value = 5.18×10(-9)).
FGF16 promotes invasive behavior of SKOV-3 ovarian cancer cells through activation of mitogen-activated protein kinase (MAPK) signaling pathway.
Roy et al., Calcutta, India. In J Biol Chem, 2014
We show that FGF16, a novel factor, is expressed in human ovary, and its expression is markedly increased in ovarian tumors.
Fgf16 is required for specification of GABAergic neurons and oligodendrocytes in the zebrafish forebrain.
Itoh et al., Kyoto, Japan. In Plos One, 2013
We examined the role of Fgf16 in the formation of the zebrafish brain.
Whole exome sequencing identifies FGF16 nonsense mutations as the cause of X-linked recessive metacarpal 4/5 fusion.
Mundlos et al., Poznań, Poland. In J Med Genet, 2013
RESULTS: Exome sequencing detected a nonsense mutation (c.C535T; p.R179X) in exon 3 of the FGF16 gene, which maps to chromosome Xq21.1.
FGF-2 and FGF-16 protect isolated perfused mouse hearts from acute doxorubicin-induced contractile dysfunction.
Cattini et al., Winnipeg, Canada. In Cardiovasc Toxicol, 2013
Pre-treatment with a non-mitogenic FGF-2 mutant or FGF-16 also protected against a doxorubicin-induced decrease in DP.
Pathophysiological roles of FGF signaling in the heart.
Ohta et al., Kyoto, Japan. In Front Physiol, 2012
In contrast, FGF16 may prevent these by competing with FGF2 for the binding site of FGFR1c.
Identification of candidate genes and mutations in QTL regions for chicken growth using bioinformatic analysis of NGS and SNP-chip data.
Marklund et al., Uppsala, Sweden. In Front Genet, 2012
The candidate mutations were identified within the GCG, IGFBP2, GRB14, CRIM1, FGF16, VEGFR-2, ALG11, EDN1, SNX6, and BIRC7 genes.
Embryonic survival and severity of cardiac and craniofacial defects are affected by genetic background in fibroblast growth factor-16 null mice.
Cattini et al., Toronto, Canada. In Dna Cell Biol, 2010
After three generations, 25% of Fgf-16(-/Y) mice survived to adulthood, which could be reversed by reducing the contribution of the C57BL/6 genetic background by back crossing to another strain.
FGF-16 is a target for adrenergic stimulation through NF-kappaB activation in postnatal cardiac cells and adult mouse heart.
Cattini et al., Winnipeg, Canada. In Cardiovasc Res, 2010
Fgf-16 gene is a target for NF-kappaB activation in the postnatal heart.
Fgf16(IRESCre) mice: a tool to inactivate genes expressed in inner ear cristae and spiral prominence epithelium.
Mansour et al., Salt Lake City, United States. In Dev Dyn, 2009
Fgf16 does not have a unique role in inner ear development and the Fgf16 lineage is found throughout the three cristae, in portions of the semicircular canal ducts, and in the cochlear spiral prominence epithelial cells
Fgf16 is required for cardiomyocyte proliferation in the mouse embryonic heart.
Itoh et al., Kyoto, Japan. In Dev Dyn, 2008
proliferation of embryonic cardiomyocytes was significantly decreased, indicating that Fgf16 is a growth factor for these cells
FGF-16 is required for embryonic heart development.
Cattini et al., Winnipeg, Canada. In Biochem Biophys Res Commun, 2008
These findings indicate FGF-16 is required for embryonic heart development in mid-gestation through its positive effect on myocardial growth.
Cancer genomics and genetics of FGFR2 (Review).
Katoh, Tokyo, Japan. In Int J Oncol, 2008
FGFR2b is a high affinity receptor for FGF1, FGF3, FGF7, FGF10 and FGF22, while FGFR2c for FGF1, FGF2, FGF4, FGF6, FGF9, FGF16 and FGF20.
Using gene expression profiling to identify the molecular basis of the synergistic actions of hepatocyte growth factor and vascular endothelial growth factor in human endothelial cells.
Hwang et al., San Francisco, United States. In Br J Pharmacol, 2003
At 4 h, the combination of the two growth factors induced a number of chemokine and cytokines and their receptors (IL-8, IL-6, IL-11, CCR6, CXCR1,CXC1 and IL17RC), numerous genes involved in growth factor signal transduction (egr-1, fosB, grb10, grb14,MAP2K3,MAP3K8, MAPKAP2,MPK3, DUSP4 and DUSP6), as well as a number of other growth factors (PDGFA, BMP2, Hb-EGF, FGF16, heuregulin beta 1, c-kit ligand, angiopoietin 2 and angiopoietin 4 and VEGFC).
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