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 (Q44683463)

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English	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	scientific article

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Europe PubMed Central

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5 December 2017

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 (English)

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Europe PubMed Central

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5 December 2017

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Ramesh Natarajan

2

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5 December 2017

6

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Paul Dent

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5 December 2017

5

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Sarah Spiegel

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5 December 2017

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Seema Gupta

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5 December 2017

Shawn G Payne

3

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5 December 2017

Elaine J Studer

4

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5 December 2017

Phillip B Hylemon

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5 December 2017

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2 December 2003

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5 December 2017

Journal of Biological Chemistry

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5 December 2017

279

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5 December 2017

7

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5 December 2017

5821-5828

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5 December 2017

Regulation of bile acid biosynthesis

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Bile acid-mediated hepatocyte apoptosis and cholestatic liver disease

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Lithocholate metabolism during chemotherapy for gallstone dissolution. 2. Absorption and sulphation

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Taurolithocholic acid-3 sulfate induces CD95 trafficking and apoptosis in a c-Jun N-terminal kinase-dependent manner

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Toxic bile salts induce rodent hepatocyte apoptosis via direct activation of Fas.

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Deoxycholic acid (DCA) causes ligand-independent activation of epidermal growth factor receptor (EGFR) and FAS receptor in primary hepatocytes: inhibition of EGFR/mitogen-activated protein kinase-signaling module enhances DCA-induced apoptosis.

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Activation and role of mitogen-activated protein kinases in deoxycholic acid-induced apoptosis

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Bile Acid Regulation of C/EBPβ, CREB, and c-Jun Function, via the Extracellular Signal-Regulated Kinase and c-Jun NH2-Terminal Kinase Pathways, Modulates the Apoptotic Response of Hepatocytes

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Activation of the Raf-1/MEK/ERK cascade by bile acids occurs via the epidermal growth factor receptor in primary rat hepatocytes

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

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The bile acid-activated phosphatidylinositol 3-kinase pathway inhibits Fas apoptosis upstream of bid in rodent hepatocytes

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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

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Bile acid induction of cytokine expression by macrophages correlates with repression of hepatic cholesterol 7alpha-hydroxylase

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

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Interleukin-10 expression is autoregulated at the transcriptional level in human and murine kupffer cells

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Jun kinase modulates tumor necrosis factor-dependent apoptosis in liver cells

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Early activation of c-Jun N-terminal kinase and p38 kinase regulate cell survival in response to tumor necrosis factor alpha

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Lymphocyte activation and capping of hormone receptors

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21 January 2018

CD95 Signaling via Ceramide-rich Membrane Rafts

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21 January 2018

Ceramide enables fas to cap and kill.

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21 January 2018

Ceramide-mediated clustering is required for CD95-DISC formation

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CD95 rapidly clusters in cells of diverse origins

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Intracellular mechanisms of L-selectin induced capping

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Co-capping of ras proteins with surface immunoglobulins in B lymphocytes

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Initiation of signal transduction through the T cell receptor requires the multivalent engagement of peptide/MHC ligands [corrected]

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Caveolins, liquid-ordered domains, and signal transduction

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Role of sphingomyelinase and ceramide in modulating rafts: do biophysical properties determine biologic outcome?

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21 January 2018

Regulation of ceramide production and apoptosis

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21 January 2018

Ultraviolet radiation-induced apoptosis is mediated by activation of CD-95 (Fas/APO-1).

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21 January 2018

Regulation of death receptor signaling and apoptosis by ceramide

1 reference

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Phenotypic stability of adult rat hepatocytes in primary monolayer culture

1 reference

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21 January 2018

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

1 reference

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21 January 2018

Tumor necrosis factor receptor and Fas signaling mechanisms.

1 reference

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21 January 2018

Bile salt-induced hepatocyte apoptosis involves epidermal growth factor receptor-dependent CD95 tyrosine phosphorylation

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21 January 2018

CD95-mediated apoptosis in vivo involves acid sphingomyelinase.

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21 January 2018

Acidic sphingomyelinase (ASM) is necessary for fas-induced GD3 ganglioside accumulation and efficient apoptosis of lymphoid cells

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Non-apoptotic Fas signaling.

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The antitumor ether lipid ET-18-OCH(3) induces apoptosis through translocation and capping of Fas/CD95 into membrane rafts in human leukemic cells

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Herpes simplex virus thymidine kinase/ganciclovir-induced apoptosis involves ligand-independent death receptor aggregation and activation of caspases.

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Ultraviolet light induces apoptosis via direct activation of CD95 (Fas/APO-1) independently of its ligand CD95L

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Glutamine deprivation-mediated cell shrinkage induces ligand-independent CD95 receptor signaling and apoptosis

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Brefeldin A: the advantage of being uncompetitive

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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

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Fas induces cytoplasmic apoptotic responses and activation of the MKK7-JNK/SAPK and MKK6-p38 pathways independent of CPP32-like proteases.

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

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Dissecting Fas signaling with an altered-specificity death-domain mutant: requirement of FADD binding for apoptosis but not Jun N-terminal kinase activation

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Ceramide: second messenger or modulator of membrane structure and dynamics?

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

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

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Apoptotic, non-apoptotic, and anti-apoptotic pathways of tumor necrosis factor signalling

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21 January 2018

Identifiers

10.1074/JBC.M310979200

1 reference

Europe PubMed Central

PubMed publication ID

5 December 2017

PubMed publication ID

1 reference

Europe PubMed Central

PubMed publication ID

5 December 2017

ResearchGate publication ID

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