anti-Golgi phosphoprotein 3 (Coat-Protein) (GOLPH3) Antibodies

Mouse (Murine) Golgi phosphoprotein 3 (Coat-Protein) (GOLPH3) interaction partners

1. Golph3 is a target gene of miR34a. miR34a/GOLPH3 axis abrogates cancer cell stemness involved in urothelial bladder cancer chemoresistance.

2. The current study found that GOLPH3, an outer membrane protein of the Golgi complex, was significantly upregulated in N2A cells upon oxygen-glucose deprivation and reoxygenation.

Human Golgi phosphoprotein 3 (Coat-Protein) (GOLPH3) interaction partners

1. Overexpression of GOLPH3 may be involved in the resistance of HT29 colon cancer cells to cisplatin chemotherapy by activating multiple cell signaling pathways.

2. High GOLPH3 expression is associated with breast cancer.

3. This study provides a brand new evidence that GOLPH3 promotes glioma cell proliferation by facilitating Wls recycling and Wnt/beta-catenin signaling.

4. High GOLPH3 expression is associated with glioma progression.

5. Proteomic-based screens identified GOLPH3 as a resident protein of the Golgi apparatus, and second as an oncogene product in a screen for genes amplified in cancer. A third screen uncovered the association of GOLPH3 with the Golgi resident phosphatidyl inositol 4 phosphate to maintain the characteristic ribbon structure of the Golgi apparatus favoring vesicular transport of secretory proteins. [review]

6. Overexpression of GOLPH3 resulted in the downregulation of p21 protein, upregulation of cyclin D1 and increased retinoblastomaassociated protein phosphorylation, consequently leading to accelerated cell cycle progression.

7. Results indicate that GOLPH3 is an independent predictive factor for neoadjuvant chemoradiotherapy (nCRT) sensitivity and prognosis in locally advanced rectal cancer (LARC).

8. Results provide evidences that overexpression of GOLPH3 stimulates EMT via the Wnt/beta-catenin signaling pathway, which further promotes metastasis of epithelial ovarian cancer.

9. GOLPH3 levels may be a novel prognostic biomarker of tobacco related lung disease.

10. Authors confirm that the decrease of GOLPH3 that promotes the apoptosis of glioma cells may be regulated by the activation of NDRG1 and cleaved capcase 3. There was a inverse association between GOLPH3 and NDRG1 in glioma samples.

11. Data found that miR-134 was highly downregulated in gastric cancer tissues and cell lines and inversely correlated with GOLPH3. These results suggest that miR-134 regulates gastric cancer cell proliferation, at least potentially, through downregulation of the GOLPH3 gene, implicating a candidate tumor-suppressor miRNA in the pathogenesis of gastric cancer.

12. In this review, we will explore the cellular functions regulated by GOLPH3 and discuss if and how they contribute to the oncogenic activity of this intriguing Golgi localized oncoprotein.

13. cumulative evidence indicates that GOLPH3 participates in several cellular processes critical for cancer cells, emerging as an attractive therapeutic target

14. GOLPH3 overexpression may participate in the occurrence and development of colorectal carcinoma by inhibiting apoptosis and promoting angiogenesis.

15. Results show that high GOLPH3 and nuclear/cytoplasmic YB-1 expression correlated with a poor prognosis in patients with prostate cancer.

16. Review/Meta-analysis: overexpression of GOLPH3 predicts poor prognosis in solid tumors.

17. GOLPH3 is likely to play important roles in bladder cancer progression via modulating AKT/mTOR signaling, and it is a novel prognostic biomarker and promising therapeutic target for bladder cancer.

18. GOLPH3 was expressed in prostate cancer cell lines. Our findings suggest GOLPH3 regulate MMP9 expression which impact cell migration and invasion.

19. GOLPH3 promotes glioblastoma cell migration and invasion via the mTOR-YB1pathway.

20. GOLPH3 expression predicts poor prognosis in patients with prostate cancer undergoing radical prostatectomy.

Cow (Bovine) Golgi phosphoprotein 3 (Coat-Protein) (GOLPH3) interaction partners

1. The selective S-nitrosylation of EMMPRIN and GOLPH3 at the Golgi apparatus in endothelial cells results from the physical proximity to eNOS-derived nitric oxide.