Asset Details
Do you wish to reserve the book?
The RSPO–LGR4/5–ZNRF3/RNF43 module controls liver zonation and size
Hey, we have placed the reservation for you!
By the way, why not check out events that you can attend while you pick your title.
Oops! Something went wrong.
Looks like we were not able to place the reservation. Kindly try again later.
Are you sure you want to remove the book from the shelf?
The RSPO–LGR4/5–ZNRF3/RNF43 module controls liver zonation and size
Do you wish to request the book?
The RSPO–LGR4/5–ZNRF3/RNF43 module controls liver zonation and size
Please be aware that the book you have requested cannot be checked out. If you would like to checkout this book, you can reserve another copy
We have requested the book for you!
Your request is successful and it will be processed during the Library working hours. Please check the status of your request in My Requests.
Oops! Something went wrong.
Looks like we were not able to place your request. Kindly try again later.
Journal Article
The RSPO–LGR4/5–ZNRF3/RNF43 module controls liver zonation and size
2016
Overview
LGR4/5 receptors and their cognate RSPO ligands potentiate Wnt/β-catenin signalling and promote proliferation and tissue homeostasis in epithelial stem cell compartments. In the liver, metabolic zonation requires a Wnt/β-catenin signalling gradient, but the instructive mechanism controlling its spatiotemporal regulation is not known. We have now identified the RSPO–LGR4/5–ZNRF3/RNF43 module as a master regulator of Wnt/β-catenin-mediated metabolic liver zonation. Liver-specific LGR4/5 loss of function (LOF) or RSPO blockade disrupted hepatic Wnt/β-catenin signalling and zonation. Conversely, pathway activation in ZNRF3/RNF43 LOF mice or with recombinant RSPO1 protein expanded the hepatic Wnt/β-catenin signalling gradient in a reversible and LGR4/5-dependent manner. Recombinant RSPO1 protein increased liver size and improved liver regeneration, whereas LGR4/5 LOF caused the opposite effects, resulting in hypoplastic livers. Furthermore, we show that LGR4
+
hepatocytes throughout the lobule contribute to liver homeostasis without zonal dominance. Taken together, our results indicate that the RSPO–LGR4/5–ZNRF3/RNF43 module controls metabolic liver zonation and is a hepatic growth/size rheostat during development, homeostasis and regeneration.
Tchorz and colleagues identify a role for the RSPO–LGR4/5–ZNRF3/RNF43 module as master regulator of Wnt/β-catenin-mediated metabolic liver zonation and hepatic growth/size control during development, homeostasis and regeneration.
Publisher
Nature Publishing Group UK,Nature Publishing Group
Subject
/ 14
/ 14/19
/ 38
/ 38/1
/ 38/32
/ 38/91
/ 45
/ 64
/ 64/110
/ 64/60
/ 82
/ 82/51
/ Animals
/ beta-Galactosidase - metabolism
/ Cellular signal transduction
/ Control
/ Cytochrome P-450 CYP2E1 - metabolism
/ Enzymes
/ Ligands
/ Liver
/ Liver - growth & development
/ Proteins
/ Receptors, G-Protein-Coupled - metabolism
/ Thrombospondins - metabolism
/ Ubiquitin-Protein Ligases - metabolism
/ Zonation
