Proteasome activation by hepatitis C core protein is reversed by ethanol-induced oxidative stress.

Proteasome activation by hepatitis C core protein is reversed by ethanol-induced oxidative stress. Research Abstract Details 

Research Abstract Table of Contents

Jump to the:

Proteasome activation by hepatitis C core protein is reversed by ethanol-induced oxidative stress. Abstract Text:

Background & Aims: The proteasome is a major cellular proteinase. Its activity is modulated by cellular oxidants. Hepatitis C core protein and ethanol exposure both cause enhanced oxidant generation. The aim was to investigate whether core protein, by its ability to generate oxidants, alters proteasome activity and whether these alterations are further affected by ethanol exposure. Methods: These interactions were examined in Huh-7 cell lines that expressed inducible HCV core protein and/or constitutive cytochrome P450 2E1 (CYP2E1) and as purified components in a cell-free system. Chymotrypsin-like proteasome activity was measured fluorometrically. Results: Proteasome activity in core-positive 191-20 cells was 20% higher than that in core-negative cells and was enhanced 3-fold in CYP2E1-expressing L14 cells. Exposure of core-positive cells to glutathione ethyl ester, catalase, or the CYP2E1 inhibitor diallyl sulfide partially reversed the elevation of proteasome activity in core-positive cells, whereas ethanol exposure suppressed proteasome activity. The results indicate that proteasome activity was up-regulated by low levels of core-induced oxidative stress but down-regulated by high levels of ethanol-elicited stress. These findings were partially mimicked in a cell-free system. Addition of core protein enhanced the peptidase activity of purified 20S proteasome containing the proteasome activator PA28 and was further potentiated by addition of liver mitochondrial and/or microsome fractions. However, proteasome activation was significantly attenuated when fractions were obtained from ethanol-fed animals. Conclusions: HCV core protein interacts with PA28, mitochondrial, and endoplasmic reticulum proteins to cause low levels of oxidant stress and proteasome activation, which is dampened during ethanol metabolism when oxidant generation is higher.

Proteasome activation by hepatitis C core protein is reversed by ethanol-induced oxidative stress. Publishing Authors By Initials

For similar abstracts research abstracts see: abstracts research

PUBMED ID PMID:

MEDLINE DATE:

Proteasome activation by hepatitis C core protein is reversed by ethanol-induced oxidative stress. Journal Published:

PUBLICATION TYPE: Journal Article

Journal: Gastroenterology

VOLUME: 134

Page Numbers: 2144-52

Journal Abbreviation: Gastroenterology

ISSN: 1528-0012

DAY: 4

MONTH: 03

YEAR: 2008

Proteasome activation by hepatitis C core protein is reversed by ethanol-induced oxidative stress. Information

Number of References:

LANGUAGE: eng

NlmUniqueID: 374630

Proteasome activation by hepatitis C core protein is reversed by ethanol-induced oxidative stress. Keywords Mesh Terms:

KEYWORDS:

MESH TERMS:

Chemical & Substance for Abstract: Proteasome activation by hepatitis C core protein is reversed by ethanol-induced oxidative stress. Information

Substance Name:

Registry Number:

Grant and Affiliation Information for Proteasome activation by hepatitis C core protein is reversed by ethanol-induced oxidative stress.

AFFILIATION: Liver Study Unit, Omaha Veterans Affairs (VA) Medical Center, Eppley Institute, University of Nebraska Medical Center, Omaha, Nebraska; Department of Internal Medicine, Eppley Institute, University of Nebraska Medical Center, Omaha, Nebraska.

Country: United States

AGENCY:

GRANT:

ACRONYM:

MEDLINETA: Gastroenterology

REFSOURCE:

DATABASENAME:

ACCESSION NUMBER:

Number Hits: 0

Proteasome activation by hepatitis C core protein is reversed by ethanol-induced oxidative stress Related Publications

• Analysis of order statistic filters applied to ultrasonic flaw detection using split-spectrum processing.
• Configurational probabilities for symmetric dimers on a lattice: an analytical approximation with exact limits at low and high densities.
• Coxsackie virus in urban sewage; recovery of virus in season of low incidence of reported poliomyelitis.
• Cushing's syndrome in children.
• Development of the bacterial photosynthetic apparatus.
• Differences in the pattern of presentation and treatment of proximal and distal gastric cancer: results of the 2001 gastric patient care evaluation.
• Examination of the effects of structured small group formats on medical students' problem-solving performance.
• How many guests, what sort of hosts?
• Hurricane-hit practice offers lessons in disaster planning.
• Identification of proteins involved in formaldehyde metabolism by Rhodobacter sphaeroides.
• Implication of altered proteasome function in alcoholic liver injury.
• Isoprene emission from plants: why and how.
• Kinetics of erythropoiesis. A comparison of response to anemia induced by phenylhydrazine and by blood loss.
• Laboratory studies on poliomyelitis, Toronto 1947.
• Maximum likelihood estimation of A-scan amplitudes for coherent targets in media of unresolvable scatterers.
• Medical Triage for WMD Incidents Incidents an adaptation of daily triage.
• Microbes in the energy grid.
• Pharmacologic interventions in chronic obstructive pulmonary disease: bronchodilators.
• Poliomyelitis virus in urban sewage; an examination for its presence over a period of 12 months.
• Prolonged survival of human poliomyelitis virus in experimentally infected river water.
• Proteasome activation by hepatitis C core protein is reversed by ethanol-induced oxidative stress.
• Rehabilitation in ankylosing spondylitis.
• Review: transient left ventricular apical ballooning, broken heart syndrome, ampulla cardiomyopathy, atypical apical ballooning, or Tako-Tsubo cardiomyopathy.
• Rh factor.
• SYSTEMIC THERAPY WITH AMETHOPTERIN IN SQUAMOUS CARCINOMA OF THE HEAD AND NECK.
• Sarcoidosis presenting as a rib fracture.
• Social profile: assessment of validity and reliability with preschool children.
• Surgically managed gastrointestinal stromal tumors: a comparative and prognostic analysis.
• Treatment of local regional disease.
• Unilateral hypersecretion of aldosterone associated with adrenal hyperplasia as a cause of primary aldosteronism.