ArticlePloS one2011
The Golgi localization of GOLPH2 (GP73/GOLM1) is determined by the transmembrane and cytoplamic sequences.
Article in PloS one, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.
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Who cites it
33 citing papers in PubMed, 56 citations in OpenAlex.
- Interaction with COPII Member SAR1 Is Critical for the Delivery ofPlants (Basel, Switzerland) · 2026Article
- A unified intracellular pH landscape with SITE-pHorin: a quantum-entanglement-enhanced pH probe.Science China. Life sciences · 2026Article
- GP73-dependent regulation of exosome biogenesis promotes colorectal cancer liver metastasis.Molecular cancer · 2025Article
- GP73 reinforces cytotoxic T-cell function by regulating HIF-1α and increasing antitumor efficacy.Journal for immunotherapy of cancer · 2025Article
- Current status and new directions for hepatocellular carcinoma diagnosis.Liver research (Beijing, China) · 2024Review
- GOLM1 promotes prostate cancer progression via interaction with PSMD1 and enhancing AR-driven transcriptional activation.Journal of cellular and molecular medicine · 2024Article
- Golgi protein 73: the driver of inflammation in the immune and tumor microenvironment.Frontiers in immunology · 2024Review
- miR-145 as a Potential Biomarker and Therapeutic Target in Patients with Non-Small Cell Lung Cancer.International journal of molecular sciences · 2023Article
- Progress in pH-Sensitive sensors: essential tools for organelle pH detection, spotlighting mitochondrion and diverse applications.Frontiers in pharmacology · 2023Review
- GP73 is a glucogenic hormone contributing to SARS-CoV-2-induced hyperglycemia.Nature metabolism · 2022Article
- GP73 is a TBC-domain Rab GTPase-activating protein contributing to the pathogenesis of non-alcoholic fatty liver disease without obesity.Nature communications · 2021Article
- GP73-mediated secretion of AFP and GP73 promotes proliferation and metastasis of hepatocellular carcinoma cells.Oncogenesis · 2021Article
- Golgi Phosphoprotein 73: The Driver of Epithelial-Mesenchymal Transition in Cancer.Frontiers in oncology · 2021Review
- Golgi protein 73, hepatocellular carcinoma and other types of cancers.Liver research (Beijing, China) · 2020Article
- Effects of hub genes on the clinicopathological and prognostic features of lung adenocarcinoma.Oncology letters · 2020Article
- GNrep mouse: A reporter mouse for front-rear cell polarity.Genesis (New York, N.Y. : 2000) · 2019Article
- Golgi protein 73 and its diagnostic value in liver diseases.Cell proliferation · 2019Review
- Golgi Membrane Protein 1 (GOLM1) Promotes Growth and Metastasis of Breast Cancer Cells via Regulating Matrix Metalloproteinase-13 (MMP13).Medical science monitor : international medical journal of experimental and clinical research · 2019Article
- A Nonsynonymous Variant in the GOLM1 Gene in Cutaneous Malignant Melanoma.Journal of the National Cancer Institute · 2018Article
- Members of the GalNAc-T family of enzymes utilize distinct Golgi localization mechanisms.Glycobiology · 2018Article
Corrections and comments
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Authors and funding
5 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Golgi phosphoprotein 2 (GOLPH2) is a resident Golgi type-II membrane protein upregulated in liver disease. Given that GOLPH2 traffics through endosomes and can be secreted into the circulation, it is a promising serum marker for liver diseases. The structure of GOLPH2 and the functions of its different protein domains are not known. In the current study, we investigated the structural determinants for Golgi localization using a panel of GOLPH2 truncation mutants. The Golgi localization of GOLPH2 was not affected by the deletion of the C-terminal part of the protein. A truncated mutant containing the N-terminal portion (the cytoplasmic tail and transmembrane domain (TMD)) localized to the Golgi. Sequential deletion analysis of the N-terminal indicated that the TMD with a positively charged residue in the cytoplasmic N-terminal tail were sufficient to support Golgi localization. We also showed that both endogenous and secreted GOLPH2 exist as a disulfide-bonded dimer, and the coiled-coil domain was sufficient for dimerization. This structural knowledge is important for the understanding the pathogenic role of GOLPH2 in liver diseases, and the development of GOLPH2-based hepatocellular cancer diagnostic methods.
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