Activation of bile acid biosynthesis by the p38 mitogen-activated protein kinase (MAPK): hepatocyte nuclear factor-4alpha phosphorylation by the p38 MAPK is required for cholesterol 7alpha-hydroxylase expression
about
Crosstalk of HNF4α with extracellular and intracellular signaling pathways in the regulation of hepatic metabolism of drugs and lipidsalpha(1)-fetoprotein transcription factor (FTF)/liver receptor homolog-1 (LRH-1) is an essential lipogenic regulatorTissue-specific activation of mitogen-activated protein kinases for expression of transthyretin by phenylalanine and its metabolite, phenylpyruvic acid.Cyclic AMP stimulates Mrp2 translocation by activating p38{alpha} MAPK in hepatic cells.INTRACELLULAR SIGNALING BY BILE ACIDS.Proteomic analysis of native hepatocyte nuclear factor-4α (HNF4α) isoforms, phosphorylation status, and interactive cofactors.Ligand-dependent regulation of the activity of the orphan nuclear receptor, small heterodimer partner (SHP), in the repression of bile acid biosynthetic CYP7A1 and CYP8B1 genes.ROCK inhibition enhances microRNA function by promoting deadenylation of targeted mRNAs via increasing PAIP2 expressionThe transcriptional activity of hepatocyte nuclear factor 4 alpha is inhibited via phosphorylation by ERK1/2.Cell signaling and nuclear receptors: new opportunities for molecular pharmaceuticals in liver disease.p38 MAPK α and β isoforms differentially regulate plasma membrane localization of MRP2.Promotion of hepatic differentiation of bone marrow mesenchymal stem cells on decellularized cell-deposited extracellular matrixBile acid signaling pathways increase stability of Small Heterodimer Partner (SHP) by inhibiting ubiquitin-proteasomal degradation.Hepatocyte nuclear factor-4α, a multifunctional nuclear receptor associated with cardiovascular disease and cholesterol catabolism.Hepatocyte nuclear factor-4alpha and bile acids regulate human concentrative nucleoside transporter-1 gene expression.Murine model of long-term obstructive jaundice.Mechanism of tissue-specific farnesoid X receptor in suppressing the expression of genes in bile-acid synthesis in mice.Bile acids increase hepatitis B virus gene expression and inhibit interferon-alpha activity.Hypoxia downregulates farnesoid X receptor via a hypoxia-inducible factor-independent but p38 mitogen-activated protein kinase-dependent pathway.The flavonoid derivative 4'-nitro-6-hydroxyflavone suppresses the activity of HNF4α and stimulates the degradation of HNF4α protein through the activation of AMPK.
P2860
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P2860
Activation of bile acid biosynthesis by the p38 mitogen-activated protein kinase (MAPK): hepatocyte nuclear factor-4alpha phosphorylation by the p38 MAPK is required for cholesterol 7alpha-hydroxylase expression
description
2007 nî lūn-bûn
@nan
2007年の論文
@ja
2007年論文
@yue
2007年論文
@zh-hant
2007年論文
@zh-hk
2007年論文
@zh-mo
2007年論文
@zh-tw
2007年论文
@wuu
2007年论文
@zh
2007年论文
@zh-cn
name
Activation of bile acid biosyn ...... 7alpha-hydroxylase expression
@ast
Activation of bile acid biosyn ...... 7alpha-hydroxylase expression
@en
type
label
Activation of bile acid biosyn ...... 7alpha-hydroxylase expression
@ast
Activation of bile acid biosyn ...... 7alpha-hydroxylase expression
@en
prefLabel
Activation of bile acid biosyn ...... 7alpha-hydroxylase expression
@ast
Activation of bile acid biosyn ...... 7alpha-hydroxylase expression
@en
P2093
P2860
P356
P1476
Activation of bile acid biosyn ...... 7alpha-hydroxylase expression
@en
P2093
Carmen M Rodriguez
Elaine J Studer
Gregorio Gil
Josephine Fernando
Olga L Tavares-Sanchez
Phillip B Hylemon
Quanzhong Li
William M Pandak
P2860
P304
24607-24614
P356
10.1074/JBC.M611481200
P407
P577
2007-06-30T00:00:00Z