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http://purl.uniprot.org/citations/33119928http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/33119928http://www.w3.org/2000/01/rdf-schema#comment"

Background and aim

Golgi protein 73 (GP73) is a transmembrane protein that can promote the proliferation of cancer cells. However, the roles of GP73 in the proliferation of non-malignant hepatocytes have rarely been investigated.

Methods

The wild-type (GP73+/+ ) and GP73 gene knockout mice (GP73-/- ) were subject to 70% partial hepatectomy (PHx) to explore the involvement of GP73 in liver regeneration.

Results

After PHx, a significant increase of GP73 expression was observed in GP73+/+ mouse liver. Noticeably, promoted recovery of liver mass was observed in GP73-/- mouse at Day 1 after PHx, as showed by the liver/body weight ratio. RNA sequencing revealed that genes relevant to cell cycle and inflammation response in the residual liver tissues were severely suppressed with the deletion of GP73, particularly the inactivation of NF-κB signal pathway in early phase of liver regeneration. In line with this, we do see the downregulation of cell cycle-related protein including cyclin D1, p-cyclin D1, β-catenin, as well as interleukin 6, tumor necrosis factor-α, CCl2, and CXCl10. In contrast, activation of mTOR signaling pathway was documented, accompanied with the histological hypertrophy of hepatocytes in GP73-/- mouse.

Conclusions

Golgi protein 73 deletion leads to delayed response of liver regeneration and inflammation in the early stages of liver regeneration after PHx."xsd:string
http://purl.uniprot.org/citations/33119928http://purl.org/dc/terms/identifier"doi:10.1111/jgh.15315"xsd:string
http://purl.uniprot.org/citations/33119928http://purl.uniprot.org/core/author"Chen X."xsd:string
http://purl.uniprot.org/citations/33119928http://purl.uniprot.org/core/author"Lu F."xsd:string
http://purl.uniprot.org/citations/33119928http://purl.uniprot.org/core/author"Qian X."xsd:string
http://purl.uniprot.org/citations/33119928http://purl.uniprot.org/core/author"Wang J."xsd:string
http://purl.uniprot.org/citations/33119928http://purl.uniprot.org/core/author"Zhang T."xsd:string
http://purl.uniprot.org/citations/33119928http://purl.uniprot.org/core/author"Wang J.'"xsd:string
http://purl.uniprot.org/citations/33119928http://purl.uniprot.org/core/author"Yao M."xsd:string
http://purl.uniprot.org/citations/33119928http://purl.uniprot.org/core/author"Ning J."xsd:string
http://purl.uniprot.org/citations/33119928http://purl.uniprot.org/core/date"2021"xsd:gYear
http://purl.uniprot.org/citations/33119928http://purl.uniprot.org/core/name"J Gastroenterol Hepatol"xsd:string
http://purl.uniprot.org/citations/33119928http://purl.uniprot.org/core/pages"1346-1356"xsd:string
http://purl.uniprot.org/citations/33119928http://purl.uniprot.org/core/title"Deletion of Golgi protein 73 delayed hepatocyte proliferation of mouse in the early stages of liver regeneration."xsd:string
http://purl.uniprot.org/citations/33119928http://purl.uniprot.org/core/volume"36"xsd:string
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