Disease relevance of Fgf9

• FGF-9 markedly stimulated both the proliferation of neointimal SMCs and the activation of extracellular signal-related kinases 1/2, effects which were abrogated by the administration of antisense FGF-9 oligonucleotides to injured arteries and the expression of the dominant negative FGFR-2 adenovirus in cultured neointimal SMCs [1].
• Non-target-derived neurotrophic substances for motoneurons including FGF-9 should be important in the pathogenesis of motor neuron disorders in the adults, especially amyotrophic lateral sclerosis [2].
• Induction of fibroblast growth factor-9 and interleukin-1alpha gene expression by motorcycle exhaust particulate extracts and benzo(a)pyrene in human lung adenocarcinoma cells [3].

Psychiatry related information on Fgf9

• Although effective delivery of exogenous FGF-9 into the central nervous system remains a problem to be solved, FGF-9 may be a promising candidate for therapeutic trials in Alzheimer disease [4].

High impact information on Fgf9

• GAF synthase catalyzed the conversion of 107 nmol of L-arginine into L-citrulline per min per mg of protein [5].
• With calmodulin and NADPH as cofactors, purified soluble GAF synthase induced an increase of 1.05 mumol of cGMP per 10(6) RFL-6 cells per 3 min per mg of protein [5].
• The soluble form of guanylyl cyclase-activating-factor (GAF) synthase from rat cerebellum was purified to homogeneity by sequential affinity chromatographic steps on adenosine 2',5'-bisphosphate (2',5'-ADP)-Sepharose and calmodulin-agarose [5].
• As was reported for fibroblasts, the IFN-gamma-regulated transcription factor GAF is phosphorylated at tyrosine after IFN-gamma treatment of HepG2 cells [6].
• Furthermore, FGF9 specifically stimulated DNA synthesis in stromal cells expressing FGFR3 [7].

Biological context of Fgf9

• These results demonstrate a directionally specific paracrine signaling from epithelial FGF9 and stromal FGFR3 [7].
• Further, FGF-9 stimulated mitogen-associated protein kinase (MAPK) phosphorylation [8].
• In both models, FGF2 and FGF9 were found to promote cellular interactions as evidenced by the extent of cellular reorganization in the coculture system, and cord morphogenesis and growth in the organotypic culture system [9].

Anatomical context of Fgf9

• Proliferation of neointimal smooth muscle cells after arterial injury. Dependence on interactions between fibroblast growth factor receptor-2 and fibroblast growth factor-9 [1].
• By whole-mount in situ hybridization, on embryonic rat spinal cord, we observed Fgf9 expression in a subpopulation of motoneurons located in the thoracic and sacral regions of the median motor column that innervate the axial muscles [10].
• FGF9 mRNA was expressed exclusively in the epithelial cells derived from well-differentiated, two-compartment Dunning R3327 rat prostate tumors [7].
• When translated in vitro, full-length FGF-9 was translocated into microsomes, glycosylated, and protected from trypsin digestion [11].
• Our results suggest that nascent FGF-9 polypeptides translocate into endoplasmic reticulum without peptide cleavage via a co-translational pathway in which both the N terminus and the central hydrophobic domain are important; thereafter, FGF-9 is glycosylated and secreted [11].

Associations of Fgf9 with chemical compounds

• Members of the series tested had n = 1.5, 4, 6, 8/9, 9, 10/11, 15, 20, 30 and 40 and were commercially available (Antarox CO series, GAF) [12].

Regulatory relationships of Fgf9

• FGF9 also failed to covalently cross-link to clonal lines of stromal cells devoid of FGFR3 that expressed FGFR1 and FGFR2IIIc [7].

Other interactions of Fgf9

• FGF-1, FGF-2, FGF-7, FGF-8, and FGF-9 were expressed in the kidney, with FGF-10 expression found only in the cortex [13].
• This localization pattern was distinct from those of aFGF, bFGF FGF-5 and FGF-9 mRNAs reported previously [14].
• FGF-5 specifically affects mesencephalic astroglial cells without changing coupling of cortical and striatal astroglia, while FGF-9 reduces gap junctional coupling in astroglia from all three brain regions [15].
• FGF-9 altered FGFR and myelin protein levels during OL differentiation; there was increased expression of FGFR-1 and decreased levels of both FGFR-2 and myelin proteins [8].

Analytical, diagnostic and therapeutic context of Fgf9

• Competition binding and immunoprecipitation assays revealed that FGF9 only bound to an FGFR on the stromal cells [7].
• FGF9 transcripts in whole rat retina were detected by RT-PCR but were not present in purified cultured Muller glia [16].
• We next examined the effects of FGF2 and FGF9 in a coculture system using 20-day-old rat SCs and PCs, and in an organotypic culture system using XY rat embryonic gonads [9].

References