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GP73 reinforces cytotoxic T-cell function by regulating HIF-1α and increasing antitumor efficacy.
J Immunother Cancer
January 2025
Department of Clinical Laboratory, The Third Medical Center of Chinese PLA General Hospital, Beijing, Beijing, China
Background: Immunotherapy that targets immune checkpoints has achieved revolutionary success, but its application in solid tumors remains limited, highlighting the need for reliable enhancement of the efficacy of immunotherapy. Golgi protein 73 (GP73), a Golgi membrane protein, has been implicated in various cellular processes, including immune regulation. Recent studies suggested that GP73 may play a role in modulating the immune response in patients with cancer.
View Article and Find Full Text PDFGP73 promotes the ox-LDL-induced inflammation in macrophages by activating the ERK/AKT pathway.
Int J Cardiol
January 2025
College of Nursing, Anhui University of Chinese Medicine, Hefei 230012, Anhui, PR China. Electronic address:
Golgi Protein 73 Promotes Angiogenesis in Hepatocellular Carcinoma.
Research (Wash D C)
July 2024
Key Laboratory of Novel Targets and Drug Study for Neural Repair of Zhejiang Province, Hangzhou City University School of Medicine, Hangzhou 310015, China.
Golgi protein 73 (GP73), a resident protein of the Golgi apparatus, is notably elevated in hepatocellular carcinoma (HCC). While its critical role in remodeling the tumor microenvironment (TME) is recognized, the intricate mechanisms are not fully understood. This study reveals that GP73 in HCC cells interacts with prolyl hydroxylase-2 (PHD-2) in a competitive manner, thereby impeding the hydroxylation of hypoxia-induced factor-1α (HIF-1α).
View Article and Find Full Text PDFDeficiency of ASGR1 promotes liver injury by increasing GP73-mediated hepatic endoplasmic reticulum stress.
Nat Commun
March 2024
Key Laboratory of Animal Genetics, Breeding and Reproduction of Shaanxi Province, College of Animal Science and Technology, Northwest A&F University, Yangling, China.
Liver injury is a core pathological process in the majority of liver diseases, yet the genetic factors predisposing individuals to its initiation and progression remain poorly understood. Here we show that asialoglycoprotein receptor 1 (ASGR1), a lectin specifically expressed in the liver, is downregulated in patients with liver fibrosis or cirrhosis and male mice with liver injury. ASGR1 deficiency exacerbates while its overexpression mitigates acetaminophen-induced acute and CCl4-induced chronic liver injuries in male mice.
View Article and Find Full Text PDFGOLM1 Promotes Pulmonary Fibrosis through Upregulation of .
Am J Respir Cell Mol Biol
March 2024
Department of Pulmonary and Critical Care Medicine and.
Idiopathic pulmonary fibrosis (IPF) is a lethal progressive disease with elusive molecular mechanisms and limited therapeutic options. Aberrant activation of fibroblasts is a central hallmark of lung fibrosis. Here, we report that Golgi membrane protein 1 (GOLM1, also known as GP73 or GOLPH2) was increased in the lungs of patients with pulmonary fibrosis and mice with bleomycin (BLM)-induced pulmonary fibrosis.
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