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SHR Neuro Krebs Kardio Lipid

Zatloukal, K; French, SW; Stumptner, C; Strnad, P; Harada, M; Toivola, DM; Cadrin, M; Omary, MB.
From Mallory to Mallory-Denk bodies: what, how and why?
EXP CELL RES. 2007; 313(10): 2033-2049.
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Autor/innen der Med Uni Graz:
Stumptner Cornelia
Zatloukal Kurt
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Abstract:
Frank B. Mallory described cytoplasmic hyaline inclusions in hepatocytes of patients with alcoholic hepatitis in 1911. These inclusions became known as Mallory bodies (MBs) and have since been associated with a variety of other liver diseases including non-alcoholic fatty liver disease. Helmut Denk and colleagues described the first animal model of MBs in 1975 that involves feeding mice griseofulvin. Since then, mouse models have been instrumental in helping understand the pathogenesis of MBs. Given the tremendous contributions made by Denk to the field, we propose renaming MBs as Mallory-Denk bodies (MDBs). The major constituents of MDBs include keratins 8 and 18 (K8/18), ubiquitin, and p62. The relevant proteins and cellular processes that contribute to MDB formation and accumulation include the type of chronic stress, the extent of stress-induced protein misfolding and consequent proteasome overload, a K8-greater-than-K18 ratio, transamidation of K8 and other proteins, presence of p62 and autophagy. Although it remains unclear whether MDBs serve a bystander, protective or injury promoting function, they do serve an important role as histological and potential progression markers in several liver diseases.
Find related publications in this database (using NLM MeSH Indexing)
Animals -
Biological Markers - analysis
Hepatocytes - metabolism
Humans - metabolism
Inclusion Bodies - metabolism
Keratins - genetics
Liver - metabolism
Liver Diseases - metabolism
Proteins - genetics
RNA-Binding Proteins - genetics
Ubiquitin - genetics

Find related publications in this database (Keywords)
ASH
chaperones
hepatocellular carcinoma
idiopathic copper toxicosis
inclusion bodies
intermediate filaments
keratins
liver disease
liver injury
NAFLD
NASH
p62
primary biliary cirrhosis
ubiquitin
Wilson disease
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