MAGI1

Official Full Name

membrane associated guanylate kinase, WW and PDZ domain containing 1

Organism

Homo sapiens

GeneID

9223

Background

The protein encoded by this gene is a member of the membrane-associated guanylate kinase homologue (MAGUK) family. MAGUK proteins participate in the assembly of multiprotein complexes on the inner surface of the plasma membrane at regions of cell-cell contact. The product of this gene may play a role as scaffolding protein at cell-cell junctions. Alternatively spliced transcript variants encoding different isoforms have been identified. [provided by RefSeq, Jul 2008]

Synonyms

AIP3; BAP1; WWP3; AIP-3; BAP-1; BAIAP1; MAGI-1; Magi1d; TNRC19; MAGI-1b;

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Detailed Information

MAGI1, also known as brain angiogenesis inhibitor associated protein 1 (BAP1), has three subtypes, MAGI1a, MAGI1b and MAGI1c, which are composed of 1139, 1171 and 1374 amino acid residues, respectively. There are also certain tissue expression and intracellular distribution specificity between different subtypes of MAGI1. MAGI1a and MAGI1c are mainly expressed in brain cells, while MAGI1b is mainly expressed in epithelial cells. MAGI1a and MAGI1b are mainly distributed in the cell membrane, and a small amount is distributed in the cytoplasm; while MAGI1c is mainly distributed in the nucleus due to its three-terminal nuclear localization sequence at the carboxy terminus.

MAGI1 showed a certain level of expression in both epithelial cells and nerve cells. Like other family members, MAGI1 consists of 5 to 6 PDZ domains, 2 WW domains, and 1 GK domain. The interaction of MAGI1 with PTEN is mediated by its PDZ2 domain.

MAGI1 and Tumor

MAGI1 is widely expressed in a variety of human tissues of almost all epithelial cell types, particularly in the human brain. Abnormal expression of MAGI1 is expressed in some cancer and human papillomavirus (HPV)-related diseases, but reports are rare. Studies have shown that in the study of the correlation between MAGI1 and malignant tumors, the down-regulation of MAGI1 activates the hippo downstream target protein YAP, which further confirms that the MAGI family may exert its anti-cancer effect by inhibiting the Hippo tumor signaling pathway.

Figure 1. A complex of MEK1, MAGI1, and PTEN regulates PIP3 turnover and AKT signaling (Zmajkovicova, et al. 2013)

MAGI1 and Colorectal Cancer

Studies have shown that immunofluorescence experiments in the colorectal cancer cell lines SW480 and HCT116 confirmed that up-regulation of MAGI1 can recruit PTEN, E-cadherin and β-catenin to the cell junction. On the one hand, it enhanced the formation of tension fibers and local adhesion plaques, which made the cell morphology flat. On the other hand, Wnt signaling pathway is down-regulated by lowering the expression level of beta-catenin in the cytoplasm, ultimately inhibiting the migration and invasion of colorectal cancer cells.

MAGI1 and Liver Cancer

In the analysis of gene expression profiles of liver cancer patients in Egypt, it was found that the expression level of MAGI1 in liver cancer patients was significantly lower than that in normal people. The results of clinical pathology showed that the expression level of MAGI1 not only has a low expression characteristic in liver cancer, but also has a certain correlation with the clinical stage of liver cancer. That is, patients with low expression of MAGI1 usually have a poor clinical stage and a short median survival time. Based on this clinical result, the researchers established a model of overexpression of the MAGI1 hepatocarcinoma cell line in the hepatocellular carcinoma cell line HepG2 for its malignant biological function experiments and molecular biological mechanisms. The results showed that overexpression of MAGI1 significantly reduced the migration and invasion of HepG2 cells, and significantly up-regulated the expression of PTEN, suggesting that MAGI1 may inhibit the invasion and migration of hepatoma cells by regulating PTEN.

MAGI1 and Cervical Cancer

Studies have found that in ZO-1 as a marker of tight junctional integrity, a tight junction loss in HPV-positive cervical cancer cells was observed with a decrease in MAGI1 expression. When the HPV E6 protein expression was inhibited, MAGI1 accumulated at the cell membrane, and zo-1 reunited, indicating a tightly connected repair. This experiment suggests that MAGI1 may be one of the HPV E6 proteins targeting recognition proteins in cervical cancer cells, and MAGI1 not only helps maintain the stability of cell junctions and cell-to-cell communication, but also induces apoptosis in polar epithelial cells. Therefore, specific mediated MAGI1 degradation may be one of the important processes in HPV infection.

References:

Vajn, K. , Plunkett, J. A. , Tapanescastillo, A. , & Oudega, M. . (2013). Axonal regeneration after spinal cord injury in zebrafish and mammals: differences, similarities, translation. Neuroscience Bulletin, 29(4), 402-410.
Chaudhry, N. , Bachelin, C. , Zujovic, V. , Hilaire, M. , Baldwin, K. T. , & Follis, R. M. , et al. (2017). Myelin-associated glycoprotein inhibits schwann cell migration and induces their death. Journal of Neuroscience the Official Journal of the Society for Neuroscience, 37(24), 5885.
Pronker, M. F. , Lemstra, S. , Snijder, J. , Heck, A. J. R. , Thies-Weesie, D. M. E. , & Pasterkamp, R. J. , et al. (2016). Structural basis of myelin-associated glycoprotein adhesion and signalling. Nature Communications, 7, 13584.

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