Discover Community Create You

Loading publication...

Noodle always counts identifier-free feature events for service operation. With your permission, Google Analytics can also estimate audience and engagement. Search text, publication identifiers, cookies, IP addresses and browser fingerprints are never included in Noodle's first-party event counters.

Privacy details

Article

Keratins let liver live: Mutations predispose to liver disease and crosslinking generates Mallory-Denk bodies.

Hepatology (Baltimore, Md.) - 1 Nov 2007

Ku Nam-On, Strnad Pavel, Zhong Bi-Hui, Tao Guo-Zhong, Omary M Bishr

Abstract excerpt

Keratin polypeptides 8 and 18 (K8/K18) are the cytoskeletal intermediate filament proteins of hepatocytes while K8/K18/K19 are the keratins of hepatobiliary ductal cells. Hepatocyte K8/K18 are highly abundant and behave as stress proteins with injury-inducible expression. Human association studies show that K8/K18 germline heterozygous mutations predispose to end-stage liver disease of multiple etiologies (...

Read the complete abstract on PubMed

Topics

Share this publication in a Topic to start or enrich a Post.

Share to Biomarkers
Share to Disease Progression
Share to Genetic Predisposition to Disease

Methodology Data sources Editorial policy Privacy Delete account & data About Contact Helena Bioinformatics

Share to Hepatocytes

Share to Liver Diseases

Share to Mutation

Share to Skin and Cellular Biology Research

Source

Identifiers

PMID: 17969036
DOI: 10.1002/hep.21976

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-08.1.

Source receipt: pubmed, retrieved 7 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence. Graph snapshot: 2026-09-29.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Keratins let liver live: Mutations predispose to liver disease and crosslinking generates Mallory-Denk bodies.PMID 17969036Read ↗

Mutation of caspase-digestion sites in keratin 18 interferes with filament reorganization, and predisposes to hepatocyte necrosis and loss of membrane integrity.Semantic proximity Read ↗

Intermediate filament proteins of digestive organs: physiology and pathophysiology.Semantic proximity Read ↗

Keratins as susceptibility genes for end-stage liver disease.Semantic proximity Read ↗

Keratin 18 overexpression but not phosphorylation or filament organization blocks mouse Mallory body formation.Semantic proximity Read ↗

Keratin hypersumoylation alters filament dynamics and is a marker for human liver disease and keratin mutation.Semantic proximity Read ↗

Keratin Mutation in Transgenic Mice Predisposes to Fas But Not Tnf–Induced Apoptosis and Massive Liver InjurySemantic proximity Read ↗

High Keratin 8/18 Ratio Predicts Aggressive Hepatocellular Cancer PhenotypeSemantic proximity Read ↗

Keratin 8 phosphorylation regulates its transamidation and hepatocyte Mallory‐Denk body formationSemantic proximity Read ↗

Keratin variants are overrepresented in primary biliary cirrhosis and associate with disease severity.Semantic proximity Read ↗

Genetic background effects of keratin 8 and 18 in a DDC-induced hepatotoxicity and Mallory-Denk body formation mouse model.Semantic proximity Read ↗

Keratin overexpression levels correlate with the extent of spontaneous pancreatic injury.Semantic proximity Read ↗

Keratin 18-deficiency results in steatohepatitis and liver tumors in old mice: A model of steatohepatitis-associated liver carcinogenesis.Semantic proximity Read ↗

⌁Select a neighboring publication to make it the new centre.