English
 
Help Privacy Policy Disclaimer
  Advanced SearchBrowse

Item

ITEM ACTIONSEXPORT
Add to Basket
  Local TagsRelease HistoryDetailsSummary

Released
Journal Article

Loss of hepatic Mboat7 leads to liver fibrosis.

MPS-Authors
/persons/resource/persons222403

Knittelfelder,  Oskar
Max Planck Institute for Molecular Cell Biology and Genetics, Max Planck Society;

/persons/resource/persons232162

Vvedenskaya,  Olga
Max Planck Institute for Molecular Cell Biology and Genetics, Max Planck Society;

/persons/resource/persons231943

Nehring,  Sophie
Max Planck Institute for Molecular Cell Biology and Genetics, Max Planck Society;

/persons/resource/persons218972

Shevchenko,  Andrej
Max Planck Institute for Molecular Cell Biology and Genetics, Max Planck Society;

External Resource
No external resources are shared
Fulltext (restricted access)
There are currently no full texts shared for your IP range.
Fulltext (public)
There are no public fulltexts stored in PuRe
Supplementary Material (public)
There is no public supplementary material available
Citation

Thangapandi, V. R., Knittelfelder, O., Brosch, M., Patsenker, E., Vvedenskaya, O., Buch, S., et al. (2020). Loss of hepatic Mboat7 leads to liver fibrosis. Gut, 70, 940-950. doi:10.1136/gutjnl-2020-320853.


Cite as: https://hdl.handle.net/21.11116/0000-0008-A2EC-7
Abstract
The rs641738C>T variant located near the membrane-bound O-acyltransferase domain containing 7 (MBOAT7) locus is associated with fibrosis in liver diseases, including non-alcoholic fatty liver disease (NAFLD), alcohol-related liver disease, hepatitis B and C. We aim to understand the mechanism by which the rs641738C>T variant contributes to pathogenesis of NAFLD.