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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Resistance to ursodeoxycholic acid-induced growth arrest can also result in resistance to deoxycholic acid-induced apoptosis and increased tumorgenicityBile acids as endogenous etiologic agents in gastrointestinal cancerPromotion of liver regeneration/repair by farnesoid X receptor in both liver and intestine in miceBile acids: regulation of apoptosis by ursodeoxycholic acidBile acids are nutrient signaling hormonesRole of interleukin-6 in Barrett's esophagus pathogenesisRole 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 microbiomeMultiple cyclin kinase inhibitors promote bile acid-induced apoptosis and autophagy in primary hepatocytes via p53-CD95-dependent signalingFarnesoid X receptor antagonizes nuclear factor kappaB in hepatic inflammatory responseBile 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 cellsSorafenib activates CD95 and promotes autophagy and cell death via Src family kinases in gastrointestinal tumor cells.Colonic inflammation and secondary bile acids in alcoholic cirrhosisDifferential regulation of EGFR-MAPK signaling by deoxycholic acid (DCA) and ursodeoxycholic acid (UDCA) in colon cancerBile 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 kinaseActivation 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 expressionHydrophobic 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 cellsTaurocholic 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 protectionVorinostat and sorafenib increase ER stress, autophagy and apoptosis via ceramide-dependent CD95 and PERK activationBCL-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.
description
2001 nî lūn-bûn
@nan
2001 թուականի Սեպտեմբերին հրատարակուած գիտական յօդուած
@hyw
2001 թվականի սեպտեմբերին հրատարակված գիտական հոդված
@hy
2001年の論文
@ja
2001年論文
@yue
2001年論文
@zh-hant
2001年論文
@zh-hk
2001年論文
@zh-mo
2001年論文
@zh-tw
2001年论文
@wuu
name
Deoxycholic acid (DCA) causes ...... nhances DCA-induced apoptosis.
@ast
Deoxycholic acid (DCA) causes ...... nhances DCA-induced apoptosis.
@en
type
label
Deoxycholic acid (DCA) causes ...... nhances DCA-induced apoptosis.
@ast
Deoxycholic acid (DCA) causes ...... nhances DCA-induced apoptosis.
@en
prefLabel
Deoxycholic acid (DCA) causes ...... nhances DCA-induced apoptosis.
@ast
Deoxycholic acid (DCA) causes ...... nhances DCA-induced apoptosis.
@en
P2093
P2860
P50
P356
P1476
Deoxycholic acid (DCA) causes ...... enhances DCA-induced apoptosis
@en
P2093
P B Fisher
P B Hylemon
R McKinstry
P2860
P304
P356
10.1091/MBC.12.9.2629
P577
2001-09-01T00:00:00Z