Golgi Membrane Protein 1 Proteins (GOLM1)

Human Golgi Membrane Protein 1 (GOLM1) interaction partners

1. serum GP73 is comparable to APRI for diagnosing significant fibrosis in children

2. The associations between Golgi membrane protein 73 (GP73) /transforming growth factor beta 1 (TGF-beta1)/SMAD2 protein (Smad2) and the clinic pathological features of patients with bladder cancer were explored.

3. These findings support GOLM1 as a candidate melanoma predisposition gene

4. GP73 is a direct target of TGF-beta1 transcriptional regulation. Its induced expression inhibits TGF-beta-Smad mediated growth suppression. On the other hand, elevated GP73 results in upregulation of ERK/Akt signaling induced by TGF-beta1.

5. GP73 is indispensable for SREBPs activation and lipogenesis. Notably, GP73 overexpression enhanced SCAP-SREBP1 binding and its Golgi trafficking even under cholesterol sufficiency.

6. serum level significantly higher in hepatocellular carcinoma patients compared to cirrhosis patients

7. GOLPH2 is a potential marker for estimating the patient's prognosis and may be a target for molecular-targeted therapy against oral squamous cell carcinoma (OSCC).

8. This article reviewed the discovery history of GP73 and summarized studies by many groups around the world, aiming at understanding its structure, expression, function, detection methods and the relationship between GP73 and liver diseases in various settings. [review]

9. Overexpressing of GOLM1 markedly promoted the tumorigenicity and metastasis of BC cells in vivo, whereas knock-down of GOLM1 caused the opposite outcomes. Results proved that GOLM1 promoted BC cell aggressiveness by regulating matrix metalloproteinase-13 (MMP13).

10. High serum GP73 expression is associated with hepatocellular carcinoma.

11. Overexpression of GP73 reversed the reduction in survival rate of hepatoma cells induced by the overexpression of miR-212 or miR-132. Conclusion

12. The important role of GP73 in regulating EMT and metastasis in HCC partly by targeting TGF-beta1/Smad2 signaling.

13. Pancreatic carcinoma and chronic pancreatitis tissues had amplified GP73expression; in response to GP73 gene silencing, carcinoma cells increased E-cadherin and decreased N-cadherin, Vimentin, and Snail expression, in addition to inhibiting the number of invasive cells, tumor volume and number of liver lesions.

14. GOLM1 acts as a critical oncogene by promoting prostate cancer cell proliferation, migration and invasion, and inhibiting apoptosis. GOLM1 plays oncogenic functions mainly through activating PI3K-AKT-mTOR signaling pathway.

15. Results showed that GOLM1 was significantly upregulated in both LUAD and LUSC tissues compared to the normal controls. However, GOLM1 expression was higher in LUAD tissues than in LUSC tissues.

16. GOLM1 was highly expressed in lung adenocarcinoma cells and associated with low survival ratio and higher grade malignancy; overexpression of GOLM1 promoted the cell proliferation.

17. PDGFA/PDGFRalpha-regulated GOLM1 promotes glioma progression possibly through activation of a key signaling kinase, AKT

18. GP73 is an effective and reliable serological marker for the diagnosis of advanced fibrosis and prediction of appearance of cirrhosis

19. GOLPH2 promotes the progression of pancreatic ductal adenocarcinoma.

20. serum GP73 is an accurate serum marker for significant fibrosis in chronic HBV infection, with higher accuracy than APRI and FIB-4. Serum GP73 is potentially a complementary tool for TE when evaluating the necessity of antiviral treatment, particularly in patients without definite antiviral indication.

Mouse (Murine) Golgi Membrane Protein 1 (GOLM1) interaction partners

1. GOLM1 expression and glutamine metabolism were suppressed by osteogenic differentiation-inducing media. GOLM1 blockage or inhibition of glutamine metabolism promoted the osteogenic differentiation of BMSCs induced by osteogenic differentiation-inducing media.

2. In Atp7b(-/-) mice, GP73 mRNA was significantly elevated at 20-46 weeks of age, coincident with extensive hepatic inflammation and fibrosis.