Independent repression of bile acid synthesis and activation of c-Jun N-terminal kinase (JNK) by activated hepatocyte fibroblast growth factor receptor 4 (FGFR4) and bile acids (Q45305228)

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English	Independent repression of bile acid synthesis and activation of c-Jun N-terminal kinase (JNK) by activated hepatocyte fibroblast growth factor receptor 4 (FGFR4) and bile acids	scientific article

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scholarly article

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Europe PubMed Central

PubMed publication ID

11 December 2017

Independent repression of bile acid synthesis and activation of c-Jun N-terminal kinase (JNK) by activated hepatocyte fibroblast growth factor receptor 4 (FGFR4) and bile acids (English)

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Europe PubMed Central

PubMed publication ID

11 December 2017

author name string

Chundong Yu

1

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Europe PubMed Central

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11 December 2017

Fen Wang

2

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11 December 2017

Chengliu Jin

3

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11 December 2017

Xinqiang Huang

4

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11 December 2017

Wallace L McKeehan

5

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Europe PubMed Central

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11 December 2017

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publication date

4 March 2005

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11 December 2017

number of pages

8

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Journal of Biological Chemistry

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11 December 2017

280

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11 December 2017

18

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11 December 2017

17707-17714

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Europe PubMed Central

PubMed publication ID

11 December 2017

Fibroblast growth factors, their receptors and signaling

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Fibroblast growth factor 19 increases metabolic rate and reverses dietary and leptin-deficient diabetes.

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Directionally specific paracrine communication mediated by epithelial FGF9 to stromal FGFR3 in two-compartment premalignant prostate tumors

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Specificity for fibroblast growth factors determined by heparan sulfate in a binary complex with the receptor kinase

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A mouse model of hepatocellular carcinoma: ectopic expression of fibroblast growth factor 19 in skeletal muscle of transgenic mice

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Elevated cholesterol metabolism and bile acid synthesis in mice lacking membrane tyrosine kinase receptor FGFR4

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Increased carbon tetrachloride-induced liver injury and fibrosis in FGFR4-deficient mice

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Mouse FGF15 is the ortholog of human and chick FGF19, but is not uniquely required for otic induction.

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FGF-19, a novel fibroblast growth factor with unique specificity for FGFR4

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The crystal structure of fibroblast growth factor (FGF) 19 reveals novel features of the FGF family and offers a structural basis for its unusual receptor affinity

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Transgenic Mice Expressing Human Fibroblast Growth Factor-19 Display Increased Metabolic Rate and Decreased Adiposity

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Definition of a novel growth factor-dependent signal cascade for the suppression of bile acid biosynthesis

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Down-regulation of cholesterol 7alpha-hydroxylase (CYP7A1) gene expression by bile acids in primary rat hepatocytes is mediated by the c-Jun N-terminal kinase pathway

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Chronic activity of ectopic type 1 fibroblast growth factor receptor tyrosine kinase in prostate epithelium results in hyperplasia accompanied by intraepithelial neoplasia

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Transgenic mouse models in carcinogenesis: interaction of c-myc with transforming growth factor alpha and hepatocyte growth factor in hepatocarcinogenesis

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Transformation and Stat activation by derivatives of FGFR1, FGFR3, and FGFR4

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CPF: an orphan nuclear receptor that regulates liver-specific expression of the human cholesterol 7alpha-hydroxylase gene

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Role of FXR and FTF in bile acid-mediated suppression of cholesterol 7alpha-hydroxylase transcription

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Molecular basis for feedback regulation of bile acid synthesis by nuclear receptors

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A regulatory cascade of the nuclear receptors FXR, SHP-1, and LRH-1 represses bile acid biosynthesis

1 reference

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Cholesterol and bile acid metabolism are impaired in mice lacking the nuclear oxysterol receptor LXR alpha

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The negative effects of bile acids and tumor necrosis factor-alpha on the transcription of cholesterol 7alpha-hydroxylase gene (CYP7A1) converge to hepatic nuclear factor-4: a novel mechanism of feedback regulation of bile acid synthesis mediated by

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Redundant pathways for negative feedback regulation of bile acid production

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Disruption of cholesterol 7alpha-hydroxylase gene in mice. I. Postnatal lethality reversed by bile acid and vitamin supplementation.

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Disruption of cholesterol 7alpha-hydroxylase gene in mice. II. Bile acid deficiency is overcome by induction of oxysterol 7alpha-hydroxylase.

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Cholic acid mediates negative feedback regulation of bile acid synthesis in mice

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FGF23, hypophosphatemia, and rickets: has phosphatonin been found?

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Autosomal dominant hypophosphataemic rickets is associated with mutations in FGF23

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Mice expressing the human CYP7A1 gene in the mouse CYP7A1 knock-out background lack induction of CYP7A1 expression by cholesterol feeding and have increased hypercholesterolemia when fed a high fat diet

1 reference

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Cholesterol feeding of mice expressing cholesterol 7alpha-hydroxylase increases bile acid pool size despite decreased enzyme activity

1 reference

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Bile acid biosynthesis

1 reference

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The enzymes, regulation, and genetics of bile acid synthesis

1 reference

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Transgenic expression of cholesterol-7-alpha-hydroxylase prevents atherosclerosis in C57BL/6J mice

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10.1074/JBC.M411771200

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Europe PubMed Central

PubMed publication ID

11 December 2017

release_t5lnx63o4bdmbhloz4inhbogcu

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24 November 2022

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PubMed publication ID

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11 December 2017

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