GLG1 and Associated Diseases
Golgi glycoprotein 1, encoded by the GLG1 gene, is a 150 kDa integral membrane glycoprotein. Current studies have found that the GLG1 protein is associated with the abnormal development of bone tissue and the progression of brain tumors. In the future, the GLG1 gene may be a potential therapeutic target. Creative Biolabs is a forward-looking large-scale gene therapy service platform. Based on the accumulation of a large amount of experience related to gene therapy, we have been continuously enriching and strengthening the ability to provide fast and reliable one-stop service for global customers.
Function of GLG1
GLG1 is located on human chromosome 16 (16q23) and contains 27 exons. The GLG1 protein, encoded by the GLG1 gene, is also known as E-selectin ligand-1 (ESL-1) and MG-160. The GLG1 protein, located inside the Golgi apparatus, is a cysteine-rich membrane sialoglycoprotein that does not contain a tyrosine kinase. GLG1 protein can bind to fibroblast growth factors (FGFs), regulate the transportation of FGFs, and participate in the signaling pathways related to FGFs. Therefore, the GLG1 protein is also known as a cysteine-rich fibroblast growth factor receptor (CFR). Mutagenesis analysis of GLG1 has shown that the GLG1 protein localized on the Golgi apparatus and the plasma membrane, respectively, can exhibit different functions through two different mechanisms. On the one hand, the C-terminus of the GLG1 protein can be fixed on the Golgi membrane, so that the GLG1 protein remains in the Golgi apparatus. On the other hand, the amount of GLG1 protein localized on the plasma membrane is controlled by its stability. The more GLG1 repeats, the more unstable the GLG1 protein is, which leads to the downregulation of GLG1 protein on the plasma membrane.
Fig.1 A two-step model for regulation of the intracellular distribution of Cfr. (Miyaoka, 2011)
GLG1-related Diseases
GLG1 knockout mice exhibit developmental delays, tail deformities, and cleft palates. Interestingly, GLG1-deficient mice were phenotypically very similar to FGF18-deficient mice and delta-like protein (Dlk) transgenic mice. Further studies have found that Dlk can negatively regulate the GLG1/FGF18 signaling pathway to hinder bone development. In addition, the expression level of GLG1 protein was correlated with different degrees of brain tumors. In low-grade astrocytomas, high levels of GLG1 protein were detected. But in malignant astrocytoma, the expression of GLG1 protein is very low. These data suggest that GLG1 protein may be involved in astrocytoma progression.
Fig.2 Phenotypes of Cfr-deficient mice. (Miyaoka, 2010)
As a high-tech enterprise, Creative Biolabs has a leading technology platform and can provide customers with personalized overall solutions. At present, the molecular mechanism of the GLG1 protein has not been elucidated clearly. If you want to tap the potential of the GLG1 gene, please contact us with your ideas. Our experts will develop a complete solution for you to expedite your progress.
References
- Miyaoka, Y.; Kato, H.; et al. Retention in the Golgi apparatus and expression on the cell surface of Cfr/Esl-1/Glg-1/MG-160 are regulated by two distinct mechanisms. Biochemical Journal. 2011. 440(1):33-41.
- Miyaoka, Y.; Tanaka, M.; et al. A novel regulatory mechanism for Fgf18 signaling involving cysteine-rich FGF receptor (Cfr) and delta-like protein (Dlk). Development. 2010. 137(1):159-167.
