Toxic bile salts induce rodent hepatocyte apoptosis via direct activation of Fas. - sprookjes - yvandenbroek - TriplyDB

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

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

http://www.wikidata.org/entity/Q33834255

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Bile acids as endogenous etiologic agents in gastrointestinal cancer Bile acid hydrophobicity is correlated with induction of apoptosis and/or growth arrest in HCT116 cells Bile acids: regulation of apoptosis by ursodeoxycholic acid The C-terminal subunit of artificially truncated human cathepsin B mediates its nuclear targeting and contributes to cell viability.Differential modulation of cellular death and survival pathways by conjugated bile acids The bile acid taurochenodeoxycholate activates a phosphatidylinositol 3-kinase-dependent survival signaling cascade Caspase-mediated cleavage of DNA topoisomerase I at unconventional sites during apoptosis An NO derivative of ursodeoxycholic acid protects against Fas-mediated liver injury by inhibiting caspase activity NF-kappaB is activated in cholestasis and functions to reduce liver injury Hepatocyte IKK2 protects Mdr2-/- mice from chronic liver failure 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 Amplification of CD95 activation by caspase 8-induced endosomal acidification in rat hepatocytes 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.Hepatocytes release ceramide-enriched pro-inflammatory extracellular vesicles in an IRE1α-dependent manner.Protective effects of neurotrophic factors on tumor necrosis factor-related apoptosis-inducing ligand (TRAIL)-mediated apoptosis of murine adrenal chromaffin cell line tsAM5D.Non-alcoholic fatty liver disease, vascular inflammation and insulin resistance are exacerbated by TRAIL deletion in mice Clinical application of transcriptional activators of bile salt transporters.Review article: mechanisms of action and therapeutic applications of ursodeoxycholic acid in chronic liver diseases.Lithocholic acid feeding results in direct hepato-toxicity independent of neutrophil function in mice Mutations to bid cleavage sites protect hepatocytes from apoptosis after ischemia/reperfusion injury Fas and Fas ligand in gut and liver.Ursodeoxycholic acid treatment of vanishing bile duct syndromes.Overexpression of mcl-1 attenuates liver injury and fibrosis in the bile duct-ligated mouse.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.The Na+/H+ exchanger controls deoxycholic acid-induced apoptosis by a H+-activated, Na+-dependent ionic shift in esophageal cells Matrix metalloproteinase inhibitor, CTS-1027, attenuates liver injury and fibrosis in the bile duct-ligated mouse.Hepatocyte death: a clear and present danger.Apoptosis in diseases of the liver.Towards specific functions of lysosomal cysteine peptidases: phenotypes of mice deficient for cathepsin B or cathepsin L.The type III inositol 1,4,5-trisphosphate receptor preferentially transmits apoptotic Ca2+ signals into mitochondria.Cathepsin B contributes to TNF-alpha-mediated hepatocyte apoptosis by promoting mitochondrial release of cytochrome c The therapeutic effects of ursodeoxycholic acid as an anti-apoptotic agent.Sustained phosphorylation of Bid is a marker for resistance to Fas-induced apoptosis during chronic liver diseases.Decreasing mitochondrial fission prevents cholestatic liver injury Bile acids induce inflammatory genes in hepatocytes: a novel mechanism of inflammation during obstructive cholestasis.Apoptosis as a mechanism for liver disease progression.Paediatric cholestatic liver disease: Diagnosis, assessment of disease progression and mechanisms of fibrogenesis.Effect of ZVAD-fmk on hepatocyte apoptosis after bile duct ligation in rat.Anti-fibrotic effect of Holothuria arenicola extract against bile duct ligation in rats.

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P2860

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

http://www.wikidata.org/entity/Q33834255

description

1999 nî lūn-bûn

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1999 թուականի Յունուարին հրատարակուած գիտական յօդուած

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1999 թվականի հունվարին հրատարակված գիտական հոդված

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1999年の論文

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1999年学术文章

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1999年学术文章

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1999年学术文章

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1999年学术文章

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1999年学术文章

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1999年學術文章

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name

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

@ast

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

@en

type

label

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

@ast

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

@en

prefLabel

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

@ast

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

@en

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Journal of Clinical Investigation

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

@en

P2093

G J Gores

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

H Miyoshi

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M E Guicciardi

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P A Svingen

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

P J Roberts

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S F Bronk

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S H Kaufmann

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W A Faubion

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P2860

Signal transduction by DR3, a death domain-containing receptor related to TNFR-1 and CD95

p28 Bap31, a Bcl-2/Bcl-XL- and procaspase-8-associated protein in the endoplasmic reticulum

CRADD, a novel human apoptotic adaptor molecule for caspase-2, and FasL/tumor necrosis factor receptor-interacting protein RIP

Involvement of MACH, a novel MORT1/FADD-interacting protease, in Fas/APO-1- and TNF receptor-induced cell death

Caspases: the executioners of apoptosis

Biochemical characteristics of caspases-3, -6, -7, and -8

Dominant-negative FADD inhibits TNFR60-, Fas/Apo1- and TRAIL-R/Apo2-mediated cell death but not gene induction

ERICE, a novel FLICE-activatable caspase

FLICE, a novel FADD-homologous ICE/CED-3-like protease, is recruited to the CD95 (Fas/APO-1) death--inducing signaling complex

Human ICE/CED-3 protease nomenclature

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137-145

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10.1172/JCI4765

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1

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103

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13405367

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9884343

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apoptotic process

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407865

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