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.

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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Q33946679

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Resistance to ursodeoxycholic acid-induced growth arrest can also result in resistance to deoxycholic acid-induced apoptosis and increased tumorgenicity Bile acids as endogenous etiologic agents in gastrointestinal cancer Promotion of liver regeneration/repair by farnesoid X receptor in both liver and intestine in mice Bile acids: regulation of apoptosis by ursodeoxycholic acid Bile acids are nutrient signaling hormones Role of interleukin-6 in Barrett's esophagus pathogenesis Role of bile acids in carcinogenesis of pancreatic cancer: An old topic with new perspective.Improved glucose metabolism following bariatric surgery is associated with increased circulating bile acid concentrations and remodeling of the gut microbiome Multiple cyclin kinase inhibitors promote bile acid-induced apoptosis and autophagy in primary hepatocytes via p53-CD95-dependent signaling Farnesoid X receptor antagonizes nuclear factor kappaB in hepatic inflammatory response 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.Bile acids initiate lineage-addicted gastroesophageal tumorigenesis by suppressing the EGF receptor-AKT axis.Differential requirement of the epidermal growth factor receptor for G protein-mediated activation of transcription factors by lysophosphatidic acid.Overexpression of mcl-1 attenuates liver injury and fibrosis in the bile duct-ligated mouse.Selective BRAFV600E inhibitor PLX4720, requires TRAIL assistance to overcome oncogenic PIK3CA resistance.Bile acids regulate hepatic gluconeogenic genes and farnesoid X receptor via G(alpha)i-protein-coupled receptors and the AKT pathway.The Na+/H+ exchanger controls deoxycholic acid-induced apoptosis by a H+-activated, Na+-dependent ionic shift in esophageal cells Sorafenib activates CD95 and promotes autophagy and cell death via Src family kinases in gastrointestinal tumor cells.Colonic inflammation and secondary bile acids in alcoholic cirrhosis Differential regulation of EGFR-MAPK signaling by deoxycholic acid (DCA) and ursodeoxycholic acid (UDCA) in colon cancer Bile acids induce inflammatory genes in hepatocytes: a novel mechanism of inflammation during obstructive cholestasis.Bile acid regulation of hepatic physiology: IV. Bile acids and death receptors.cAMP-guanine exchange factor protection from bile acid-induced hepatocyte apoptosis involves glycogen synthase kinase regulation of c-Jun NH2-terminal kinase 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 Hydrophobic bile acid apoptosis is regulated by sphingosine-1-phosphate receptor 2 in rat hepatocytes and human hepatocellular carcinoma cells.Ligand-Independent Activation of Platelet-Derived Growth Factor Receptor β during Human Immunodeficiency Virus-Transactivator of Transcription and Cocaine-Mediated Smooth Muscle Hyperplasia.The human gut sterolbiome: bile acid-microbiome endocrine aspects and therapeutics.The transcriptional activity of hepatocyte nuclear factor 4 alpha is inhibited via phosphorylation by ERK1/2.Novel insight into mechanisms of cholestatic liver injury.Bile acids regulate intestinal cell proliferation by modulating EGFR and FXR signaling.Vorinostat and sorafenib synergistically kill tumor cells via FLIP suppression and CD95 activation.Novel interaction of bile acid and neural signaling in the regulation of cholangiocyte function.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.Deoxycholic acid mediates non-canonical EGFR-MAPK activation through the induction of calcium signaling in colon cancer cells Taurocholic acid metabolism by gut microbes and colon cancer.Bile acids promote diethylnitrosamine-induced hepatocellular carcinoma via increased inflammatory signaling.Bile-acid-induced cell injury and protection Vorinostat and sorafenib increase ER stress, autophagy and apoptosis via ceramide-dependent CD95 and PERK activation BCL-2 family inhibitors enhance histone deacetylase inhibitor and sorafenib lethality via autophagy and overcome blockade of the extrinsic pathway to facilitate killing.

P2860

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P2860

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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http://www.wikidata.org/entity/Q33946679

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2001 nî lūn-bûn

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2001 թուականի Սեպտեմբերին հրատարակուած գիտական յօդուած

@hyw

2001 թվականի սեպտեմբերին հրատարակված գիտական հոդված

@hy

2001年の論文

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2001年論文

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2001年論文

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2001年論文

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2001年論文

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2001年论文

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