Golgi phosphoprotein 3 (Coat-Protein) (GOLPH3) ELISA Kits

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 is associated with the development of papillary thyroid carcinoma (PTC) and poor prognosis in patients with PTC

2. GOLPH3 increases the sensitivity of glioma cells to gefitinib.

3. GOLPH3 knockdown reduced the tumor growth rate

4. The level of JAK2, STAT3 and GOLPH3 were significantly up-regulated and exhibited pairwise correlation in human glioma tissues. The level of p-JAK2 and p-STAT3, as well as the mRNA and protein levels of cyclin D1 and c-myc, two target genes of STAT3, decreased after GOLPH3 down-regulation, while they increased after GOLPH3 over-expression both in U251 and U87 cells.

5. Data suggest that golgi phosphoprotein 3 coat protein (GOLPH3) expression in cumulus granulosa cells may facilitate the selection of top-quality eggs and embryos, the prediction of the clinical pregnancy outcomes of ICSI, and the increase of the pregnancy rate.

6. The current study suggests that GOLPH3 contributes to the tumorigenesis of hepatocellular carcinoma

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

8. High GOLPH3 expression is associated with breast cancer.

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

10. High GOLPH3 expression is associated with glioma progression.

11. 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]

12. 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.

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

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

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

16. 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.

17. 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.

18. 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.

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

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

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.