Comprehensive proteomics analysis of autophagy-deficient mouse liver.

Comprehensive proteomics analysis of autophagy-deficient mouse liver. Research Abstract Details 

Research Abstract Table of Contents

Jump to the:

Comprehensive proteomics analysis of autophagy-deficient mouse liver. Abstract Text:

Naomi Matsumoto,Junji Ezaki,Masaaki Komatsu,Katsuyuki Takahashi,Reiko Mineki,Hikari Taka,Mika Kikkawa,Tsutomu Fujimura,Mitsue Takeda-Ezaki,Takashi Ueno,Keiji Tanaka,Eiki Kominami,

Autophagy is a bulk protein degradation system for the entire organelles and cytoplasmic proteins. Previously, we have shown the liver dysfunction by autophagy deficiency. To examine the pathological effect of autophagy deficiency, we examined protein composition and their levels in autophagy-deficient liver by the proteomic analysis. While impaired autophagy led to an increase in total protein mass, the protein composition was largely unchanged, consistent with non-selective proteins/organelles degradation of autophagy. However, a series of oxidative stress-inducible proteins, including glutathione S-transferase families, protein disulfide isomerase and glucose-regulated proteins were specifically increased in autophagy-deficient liver, probably due to enhanced gene expression, which is induced by accumulation of Nrf2 in the nuclei of mutant hepatocytes. Our results suggest that autophagy deficiency causes oxidative stress, and such stress might be the main cause of liver injury in autophagy-deficient liver.

Comprehensive proteomics analysis of autophagy-deficient mouse liver. Publishing Authors By Initials

N Matsumoto,J Ezaki,M Komatsu,K Takahashi,R Mineki,H Taka,M Kikkawa,T Fujimura,M Takeda-Ezaki,T Ueno,K Tanaka,E Kominami,

For similar abstracts research abstracts see: abstracts research

PUBMED ID PMID:

MEDLINE DATE:

Comprehensive proteomics analysis of autophagy-deficient mouse liver. Journal Published:

PUBLICATION TYPE: Research Support, Non-U.S. Gov

Journal: Biochemical and biophysical research communication

VOLUME: 368

Page Numbers: 643-9

Journal Abbreviation: Biochem. Biophys. Res. Commun.

ISSN: 1090-2104

DAY: 4

MONTH: 02

YEAR: 2008

Comprehensive proteomics analysis of autophagy-deficient mouse liver. Information

Number of References:

LANGUAGE: eng

NlmUniqueID: 372516

Comprehensive proteomics analysis of autophagy-deficient mouse liver. Keywords Mesh Terms:

KEYWORDS:

MESH TERMS:

Chemical & Substance for Abstract: Comprehensive proteomics analysis of autophagy-deficient mouse liver. Information

Substance Name:

Registry Number:

Grant and Affiliation Information for Comprehensive proteomics analysis of autophagy-deficient mouse liver.

AFFILIATION: Department of Biochemistry, Juntendo University School of Medicine, 2-1-1 Hongo Bunkyo-ku, Tokyo, Japan.

Country: United States

AGENCY:

GRANT:

ACRONYM:

MEDLINETA: Biochem Biophys Res Commun

REFSOURCE:

DATABASENAME:

ACCESSION NUMBER:

Number Hits: 0

Comprehensive proteomics analysis of autophagy-deficient mouse liver Related Publications

• Analysis of where and which types of proteinases participate in lysosomal proteinase processing using bafilomycin A1 and Helicobacter pylori Vac A toxin.
• Anti-Sm autoantibodies cross-react with ribosomal protein S10: a common structural unit shared by the small nuclear RNP proteins and the ribosomal protein.
• Comprehensive proteomics analysis of autophagy-deficient mouse liver.
• Decreased lysosomal subunit c-degrading activity in fibroblasts from patients with late infantile neuronal ceroid lipofuscinosis.
• Effect of Bcl11b genotypes and gamma-radiation on the development of mouse thymic lymphomas.
• Fed-batch culture automated by uses of continuously measured cell concentration and culture volume.
• Formation of a triple-stranded DNA between d(GGA:TCC) repeats and d(GGA) repeat oligonucleotides.
• Function of the propeptide region in recombinant expression of active procathepsin L in Escherichia coli.
• Hemoprotein H-450 identified as a form of cytochrome P-450 having an endogenous ligand at the 6th coordination position of the heme.
• Initial observation of potential factors involved in the specification process of oral-aboral axis in the sand dollar Scaphechinus mirabilis.
• LC3 and Autophagy.
• Loss of Pten, a tumor suppressor, causes the strong inhibition of autophagy without affecting LC3 lipidation.
• Suppression of lysosomal proteolysis at three different steps in regenerating rat liver.
• Transcription of mouse ribosomal RNA gene with inactive extracts is activated by NAD+ in vitro.
• Tripeptidyl peptidase I, the late infantile neuronal ceroid lipofuscinosis gene product, initiates the lysosomal degradation of subunit c of ATP synthase.
• Two mouse hypervariable minisatellites: chromosomal location and simultaneous mutation.