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http://purl.uniprot.org/citations/19229075http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/19229075http://www.w3.org/2000/01/rdf-schema#comment"Fibroblast growth factor 1 (FGF-1) enhances apolipoprotein E (apoE) expression and apoE-HDL biogenesis in autocrine fashion in astrocytes (Ito, J., Y. Nagayasu, R. Lu, A. Kheirollah, M. Hayashi, and S. Yokoyama. Astrocytes produce and secrete FGF-1, which promotes the production of apoE-HDL in a manner of autocrine action. J. Lipid Res. 2005. 46: 679-686) associated with healing of brain injury (Tada,T., J-i. Ito, M. Asai, and S. Yokoyama. Fibroblast growth factor 1 is produced prior to apolipoprotein E in the astrocytes after cryo-injury of mouse brain. Neurochem. Int. 2004. 45: 23-30). FGF-1 stimulates mitogen-activated protein kinase kinase/extracellular signal-regulated kinase (MEK/ERK) to increase cholesterol biosynthesis and phosphatidylinositol 3-OH kinase (PI3K)/Akt to enhance apoE-HDL secretion (Ito, J., Y. Nagayasu, K. Okumura-Noji, R. Lu, T. Nishida, Y. Miura, K. Asai, A. Kheirollah, S. Nakaya, and S. Yokoyama. Mechanism for FGF-1 to regulate biogenesis of apoE-HDL in astrocytes. J. Lipid Res. 2007. 48: 2020-2027). We investigated the mechanism for FGF-1 to upregulate apoE transcription. FGF-1 increased apoE and liver X receptor alpha (LXRalpha) mRNAs in rat astrocytes. Increase of LXRalpha mRNA was suppressed by inhibition of the FGF-1 receptor-1 and MEK/ERK but not by inhibition of PI3K/Akt. The increases of apoE mRNA and apoE-HDL secretion were both inhibited by downregulation or inhibition of LXRalpha, while they were partially suppressed by inhibiting cholesterol biosynthesis. We identified the liver X receptor element responsible for activation of the rat apoE promoter by FGF-1 located between -450 and -320 bp, and the direct repeat 4 (DR4) element in this region (-448 to -433 bp) was responsible for the activation. Chromatin immunoprecipitation analysis supported that FGF-1 enhanced association of LXR with the rat apoE promoter. FGF-1 partially activated the apoE promoter even in the presence of an MEK inhibitor that inhibits the FGF-1-mediated enhancement of cholesterol biosynthesis. On the other hand, FGF-1 induced production of 25-hydroxycholesterol by MEK/ERK as an sterol regulatory element-dependent reaction besides cholesterol biosynthesis. We concluded that FGF-1-induced apoE expression in astrocytes depends on LXRalpha being mediated by both LXRalpha expression and an LXRalpha ligand biosynthesis."xsd:string
http://purl.uniprot.org/citations/19229075http://purl.org/dc/terms/identifier"doi:10.1194/jlr.m800594-jlr200"xsd:string
http://purl.uniprot.org/citations/19229075http://purl.uniprot.org/core/author"Ito J."xsd:string
http://purl.uniprot.org/citations/19229075http://purl.uniprot.org/core/author"Lu R."xsd:string
http://purl.uniprot.org/citations/19229075http://purl.uniprot.org/core/author"Yokoyama S."xsd:string
http://purl.uniprot.org/citations/19229075http://purl.uniprot.org/core/author"Iwamoto N."xsd:string
http://purl.uniprot.org/citations/19229075http://purl.uniprot.org/core/author"Nishimaki-Mogami T."xsd:string
http://purl.uniprot.org/citations/19229075http://purl.uniprot.org/core/date"2009"xsd:gYear
http://purl.uniprot.org/citations/19229075http://purl.uniprot.org/core/name"J Lipid Res"xsd:string
http://purl.uniprot.org/citations/19229075http://purl.uniprot.org/core/pages"1156-1164"xsd:string
http://purl.uniprot.org/citations/19229075http://purl.uniprot.org/core/title"FGF-1 induces expression of LXRalpha and production of 25-hydroxycholesterol to upregulate the apoE gene in rat astrocytes."xsd:string
http://purl.uniprot.org/citations/19229075http://purl.uniprot.org/core/volume"50"xsd:string
http://purl.uniprot.org/citations/19229075http://www.w3.org/2004/02/skos/core#exactMatchhttp://purl.uniprot.org/pubmed/19229075
http://purl.uniprot.org/citations/19229075http://xmlns.com/foaf/0.1/primaryTopicOfhttps://pubmed.ncbi.nlm.nih.gov/19229075
http://purl.uniprot.org/uniprot/P05230#attribution-B5A249A2C4F724179E2E2A7A3FA84455http://purl.uniprot.org/core/sourcehttp://purl.uniprot.org/citations/19229075
http://purl.uniprot.org/uniprot/Q04589#attribution-F68478981D5B30FCAA9E6182F418DB8Dhttp://purl.uniprot.org/core/sourcehttp://purl.uniprot.org/citations/19229075
http://purl.uniprot.org/uniprot/Q13133#attribution-B5A249A2C4F724179E2E2A7A3FA84455http://purl.uniprot.org/core/sourcehttp://purl.uniprot.org/citations/19229075
http://purl.uniprot.org/uniprot/#_A0A8J8YIL8-mappedCitation-19229075http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/19229075
http://purl.uniprot.org/uniprot/#_F1LM54-mappedCitation-19229075http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/19229075
http://purl.uniprot.org/uniprot/#_Q63827-mappedCitation-19229075http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/19229075
http://purl.uniprot.org/uniprot/#_Q04589-mappedCitation-19229075http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/19229075
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http://purl.uniprot.org/uniprot/Q04589http://purl.uniprot.org/core/mappedCitationhttp://purl.uniprot.org/citations/19229075