Deoxycholic acid activates the c-Jun N-terminal kinase pathway via FAS receptor activation in primary hepatocytes. Role of acidic sphingomyelinase-mediated ceramide generation in FAS receptor activation.

Deoxycholic acid activates the c-Jun N-terminal kinase pathway via FAS receptor activation in primary hepatocytes. Role of acidic sphingomyelinase-mediated ceramide generation in FAS receptor activation.

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Bile acids: regulation of apoptosis by ursodeoxycholic acid Bile acids: regulation of synthesis Bile acid signaling in metabolic disease and drug therapy Multiple cyclin kinase inhibitors promote bile acid-induced apoptosis and autophagy in primary hepatocytes via p53-CD95-dependent signaling Hydrophobic bile salts trigger ceramide formation through endosomal acidification Phosphatidylinositol-3-kinase p110γ contributes to bile salt-induced apoptosis in primary rat hepatocytes and human hepatoma cells Farnesoid X receptor is essential for normal glucose homeostasis Deoxycholate, an endogenous cytotoxin/genotoxin, induces the autophagic stress-survival pathway: implications for colon carcinogenesis.Overexpression of mcl-1 attenuates liver injury and fibrosis in the bile duct-ligated mouse.Acidic sphingomyelinase controls hepatic stellate cell activation and in vivo liver fibrogenesis Sorafenib activates CD95 and promotes autophagy and cell death via Src family kinases in gastrointestinal tumor cells.INTRACELLULAR SIGNALING BY BILE ACIDS.Bile acid signaling in lipid metabolism: metabolomic and lipidomic analysis of lipid and bile acid markers linked to anti-obesity and anti-diabetes in mice.Decreasing mitochondrial fission prevents cholestatic liver injury Fusobacterium and Escherichia: models of colorectal cancer driven by microbiota and the utility of microbiota in colorectal cancer screening.Hydrophobic bile acid apoptosis is regulated by sphingosine-1-phosphate receptor 2 in rat hepatocytes and human hepatocellular carcinoma cells.Translational biomarkers of acetaminophen-induced acute liver injury Bile Acid Receptors and Liver Cancer.Vorinostat and sorafenib synergistically kill tumor cells via FLIP suppression and CD95 activation.Mitogen-activated protein kinase kinase 1/2 inhibitors and 17-allylamino-17-demethoxygeldanamycin synergize to kill human gastrointestinal tumor cells in vitro via suppression of c-FLIP-s levels and activation of CD95.Pharmacology of bile acid receptors: Evolution of bile acids from simple detergents to complex signaling molecules.Bile acids promote diethylnitrosamine-induced hepatocellular carcinoma via increased inflammatory signaling.Vorinostat and sorafenib increase ER stress, autophagy and apoptosis via ceramide-dependent CD95 and PERK activation Bile acids as regulatory molecules.c-Jun N-terminal kinase 1/c-Jun activation of the p53/microRNA 34a/sirtuin 1 pathway contributes to apoptosis induced by deoxycholic acid in rat liver.Ceramide formation mediated by acid sphingomyelinase facilitates endosomal escape of caliciviruses.Vorinostat and sorafenib increase CD95 activation in gastrointestinal tumor cells through a Ca(2+)-de novo ceramide-PP2A-reactive oxygen species-dependent signaling pathway.Keratin impact on PKCδ- and ASMase-mediated regulation of hepatocyte lipid raft size - implication for FasR-associated apoptosis.Oral administration of the Aureobasidium pullulans-derived β-glucan effectively prevents the development of high fat diet-induced fatty liver in mice.Role of caspases in CD95-induced biphasic activation of acid sphingomyelinase.Role of bile acids in liver injury and regeneration following acetaminophen overdose.Regulation of autophagy by ceramide-CD95-PERK signaling.Bile acid flux through portal but not peripheral veins inhibits CYP7A1 expression without involvement of ileal FGF19 in rabbits.The constitutive androstane receptor and pregnane X receptor function coordinately to prevent bile acid-induced hepatotoxicity.Loss of cellular FLICE-inhibitory protein promotes acute cholestatic liver injury and inflammation from bile duct-ligation.Bile acids as global regulators of hepatic nutrient metabolism Endosomal Acidification and Activation of NADPH Oxidase Isoforms Are Upstream Events in Hyperosmolarity-induced Hepatocyte Apoptosis

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P2860

Deoxycholic acid activates the c-Jun N-terminal kinase pathway via FAS receptor activation in primary hepatocytes. Role of acidic sphingomyelinase-mediated ceramide generation in FAS receptor activation.

Item

http://www.wikidata.org/entity/Q44683463

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2003 nî lūn-bûn

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2003年の論文

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2003年学术文章

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2003年学术文章

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2003年学术文章

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2003年学术文章

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2003年学术文章

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2003年學術文章

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2003年學術文章

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2003年學術文章

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name

Deoxycholic acid activates the ...... on in FAS receptor activation.

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Deoxycholic acid activates the ...... on in FAS receptor activation.

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type

Item

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Deoxycholic acid activates the ...... on in FAS receptor activation.

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Deoxycholic acid activates the ...... on in FAS receptor activation.

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Deoxycholic acid activates the ...... on in FAS receptor activation.

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Deoxycholic acid activates the ...... on in FAS receptor activation.

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P1476

Deoxycholic acid activates the ...... on in FAS receptor activation.

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P2093

Elaine J Studer

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Phillip B Hylemon

http://www.w3.org/2001/XMLSchema#string

Seema Gupta

http://www.w3.org/2001/XMLSchema#string

Shawn G Payne

http://www.w3.org/2001/XMLSchema#string

P2860

Direct evidence for an important role of sphingomyelinase in ultraviolet-induced activation of c-Jun N-terminal kinase

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

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

Daxx, a novel Fas-binding protein that activates JNK and apoptosis

The bile acid taurochenodeoxycholate activates a phosphatidylinositol 3-kinase-dependent survival signaling cascade

Oocyte apoptosis is suppressed by disruption of the acid sphingomyelinase gene or by sphingosine-1-phosphate therapy

The cardiac Fas (APO-1/CD95) Receptor/Fas ligand system : relation to diastolic wall stress in volume-overload hypertrophy in vivo and activation of the transcription factor AP-1 in cardiac myocytes

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

Bile acid regulation of C/EBPbeta, CREB, and c-Jun function, via the extracellular signal-regulated kinase and c-Jun NH2-terminal kinase pathways, modulates the apoptotic response of hepatocytes.

Natural ceramide reverses Fas resistance of acid sphingomyelinase(-/-) hepatocytes.

P304

5821-5828

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scholarly article

P356

10.1074/JBC.M310979200

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English

P433

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279

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Sarah Spiegel

Ramesh Natarajan

Paul Dent

P577

2003-12-02T00:00:00Z

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P5875

8971461

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14660582

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Deoxycholic acid activates the c-Jun N-terminal kinase pathway via FAS receptor activation in primary hepatocytes. Role of acidic sphingomyelinase-mediated ceramide generation in FAS receptor activation.

about

P2860

P2860

Deoxycholic acid activates the c-Jun N-terminal kinase pathway via FAS receptor activation in primary hepatocytes. Role of acidic sphingomyelinase-mediated ceramide generation in FAS receptor activation.

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