MAGI3

更新于：2025-01-23

基本信息

别名

KIAA1634、MAGI-3、MAGI3

+ [3]

简介

Acts as a scaffolding protein at cell-cell junctions, thereby regulating various cellular and signaling processes. Cooperates with PTEN to modulate the kinase activity of AKT1. Its interaction with PTPRB and tyrosine phosphorylated proteins suggests that it may link receptor tyrosine phosphatase with its substrates at the plasma membrane. In polarized epithelial cells, involved in efficient trafficking of TGFA to the cell surface. Regulates the ability of LPAR2 to activate ERK and RhoA pathways. Regulates the JNK signaling cascade via its interaction with FZD4 and VANGL2.

关联

100 项与 MAGI3 相关的临床结果

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100 项与 MAGI3 相关的转化医学

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0 项与 MAGI3 相关的专利（医药）

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项与 MAGI3 相关的文献（医药）

2024-12-01·Inflammation

CARMA3 Drives NF-κB Activation and Promotes Intervertebral Disc Degeneration: Involvement of CARMA3-BCL10-MALT1 Signalosome

Article

作者: Zhang, Guiqi ; Meng, Yi ; Liu, Yadong ; Hu, Jianyu ; Wu, Jiani ; Fu, Hao ; Yang, Dongfang

Intervertebral disc degeneration (IDD) diseases are common and frequent diseases in orthopedics. The caspase recruitment domain (CARD) and membrane-associated guanylate kinase-like protein 3 (CARMA3) is crucial in the activation of the NF-κB pathway. However, the biological function of CARMA3 in IDD remains unknown. Here, CARMA3 expression was elevated in nucleus pulposus (NP) tissues of IDD rats and nutrient deprivation (ND)-induced NP cells. The main pathological manifestations observed in IDD rats were shrinkage of the NP, reduction of NP cells, fibrosis of NP tissues, and massive reduction of proteoglycans. These changes were accompanied by a decrease in the expression of collagen II and aggrecan, an increase in the expression of the extracellular matrix (ECM) catabolic proteases MMP-3, MMP-13, and metalloprotease with ADAMTS-5, and an increase in the activity of the pro-apoptotic protease caspase-3. The expression of p-IκBα^Ser32/36 and p-p65^Ser536 was also upregulated. However, these effects were reversed with the knockdown of CARMA3. Mechanistically, CARMA3 bound to BCL10 and MALT1 to form a signalosome. Knockdown of CARMA3 reduced the CARMA3-BCL10-MALT1 signalosome-mediated NF-κB activation. CARMA3 activated the NF-κB signaling pathway in a manner that bound to BCL10 and MALT1 to form a signalosome, which affects NP cell damage and is involved in the development of IDD. This supports CARMA3-BCL10-MALT1-NF-κB as a promising targeting axis for the treatment of IDD.

2024-09-01·Analytica Chimica Acta

Benchmark N-glycoproteomics study of common differential tissue and serum N-glycoproteins of patients with hepatocellular carcinoma

Article

作者: Bi, Ming ; Tian, Zhixin ; Bai, Bing ; Gao, Ke

For hepatocellular carcinoma (HCC), N-glycosylation has been proved to be widely involved in various aspects of the disease, including development, metastasis, subtyping, diagnosis and prognosis. The common practice is to discover biomarkers in situ of cancer occurrence (i.e., cancer vs. adjacent tissues) yet to clinically monitor in sera because of non-invasiveness. This study benchmarks N-glycoproteomics characterization of common differential tissue and serum N-glycoproteins of patients with HCC. Differential N-glycosylation in matched tissue and serum samples from the same patients were quantitatively characterized at the intact N-glycopeptide molecular level, and 29 common N-glycoproteins were found. Subcellular localization analysis was carried out to confirm the tissue originality. Secreted N-glycoprotein APOH was up-regulated, and transmembrane and intracellular N-glycoproteins including OSMR, GAT2, CSF-1 and MAGI3 were down-regulated.

2024-08-02·Cancer Discovery

St. Jude Survivorship Portal: Sharing and Analyzing Large Clinical and Genomic Datasets from Pediatric Cancer Survivors

Article

作者: Yasui, Yutaka ; Bhakta, Nickhill ; Acić, Aleksandar ; Zhang, Jinghui ; Wang, Zhaoming ; Shelton, Kyla ; Wang, Fan ; Ness, Kirsten K. ; Sandor, Stephanie R. ; Im, Cindy ; Sapkota, Yadav ; Matt, Gavriel Y. ; Zhou, Xin ; Sioson, Edgar ; Paul, Robin ; Gangwani, Karishma ; McLeod, Clay ; Liu, Qi ; Zaldivar Peraza, Airen ; Armstrong, Gregory T. ; Hudson, Melissa M. ; Patel, Jaimin ; Reilly, Colleen ; Lu, Congyu ; Robison, Leslie L. ; Wang, Jian ; Wilson, Carmen L.

AbstractChildhood cancer survivorship studies generate comprehensive datasets comprising demographic, diagnosis, treatment, outcome, and genomic data from survivors. To broadly share this data, we created the St. Jude Survivorship Portal (https://survivorship.stjude.cloud), the first data portal for sharing, analyzing, and visualizing pediatric cancer survivorship data. More than 1,600 phenotypic variables and 400 million genetic variants from more than 7,700 childhood cancer survivors can be explored on this free, open-access portal. Summary statistics of variables are computed on-the-fly and visualized through interactive and customizable charts. Survivor cohorts can be customized and/or divided into groups for comparative analysis. Users can also seamlessly perform cumulative incidence and regression analyses on the stored survivorship data. Using the portal, we explored the ototoxic effects of platinum-based chemotherapy, uncovered a novel association between mental health, age, and limb amputation, and discovered a novel haplotype in MAGI3 strongly associated with cardiomyopathy specifically in survivors of African ancestry.Significance: The St. Jude Survivorship Portal is the first data portal designed to share and explore clinical and genetic data from childhood cancer survivors. The portal provides both open- and controlled-access features and will fulfill a wide range of data sharing needs of the survivorship research community and beyond.

项与 MAGI3 相关的新闻（医药）

2022-08-17

·生物谷

Molecular Cancer: E3泛素连接酶MAGI3可以预测结直肠癌化疗疗效

结直肠癌是第三种最常见的癌症，也是与癌症相关的死亡的第四大常见原因，2018年估计有180万新病例和88万人归因于死亡。结直肠癌是第三种最常见的癌症，也是与癌症相关的死亡的第四大常见原因，2018年估计有180万新病例和88万人归因于死亡。结直肠癌的预后与确诊时的分期有关，I期约90%，II期约70%，III期约58%，IV期不到15%。复发和化疗耐药是结直肠癌(CRC)的主要死亡原因。因此，阐明结直肠癌的潜在机制并找出预测因素，为改善结直肠癌的预后量身定做辅助化疗具有重要意义。图片来源: https://doi.org/10.1186/s12943-022-01622-9 近日，来自首都医科大学的研究者们在Molecular Cancer杂志上发表了题为“E3 ubiquitin ligase MAGI3 degrades c-Myc and acts as a predictor for chemotherapy response in colorectal cancer”的文章，该研究揭示了MAGI3是一种新的E3泛素连接酶，通过降解c-Myc来调节结直肠癌的发生发展，可能成为结直肠癌患者辅助化疗的潜在预测指标。在本研究中，研究者通过筛选差异表达基因(DEG)、构建随机森林分类和对DEGS的重要性进行排序，研究者确定膜相关鸟氨酸激酶、WW和PDZ结构域3(MAGI3)是影响结直肠癌复发的重要基因。免疫组织化学和免疫印迹法进一步检测MAGI3在结直肠癌组织和细胞系中的表达。采用细胞计数试剂盒8、平板集落形成法、流式细胞仪、皮下注射法和偶氮甲烷加葡聚糖硫酸钠诱导小鼠结直肠癌实验，探讨MAGI3对结直肠癌细胞增殖、生长、细胞周期、细胞凋亡、异种移植瘤形成和化疗耐药性的影响。通过基因集浓缩分析、实时定量聚合酶链式反应、免疫印迹、免疫共沉淀、泛素化、GST融合蛋白下拉和免疫组织化学染色等方法，进一步探讨其可能的分子机制。本研究结果表明，MAGI3表达异常与结直肠癌复发和预后不良有关。MAGI3是Skp1-cullin E3连接酶的一个新的底物结合亚基，可以识别c-Myc，并参与c-Myc的泛素化和降解。MAGI3在结直肠癌细胞中的表达通过抑制c-Myc的激活，在体内外抑制细胞生长，促进细胞凋亡，增加对氟嘧啶类化疗药物的敏感性。在临床上，MAGI3高表达的II/III期大肠癌患者无复发生存率显著提高(约80%，5年)，且不需要进一步的辅助化疗。含MAGI3的患者在以氟嘧啶为基础的化疗中有很好的缓解率或无复发生存率，建议接受以氟嘧啶为基础的辅助化疗。 E3泛素连接酶MAGI3降解c-Myc预测结直肠癌化疗疗效图片来源: https://doi.org/10.1186/s12943-022-01622-9 综上所述，本研究确定MAGI3是结直肠癌中的一种新的肿瘤抑制因子，并证明了它通过靶向c-Myc来抑制增殖。本研究首次提供了令人信服的证据，证明MAGI3是一种新的E3泛素连接酶，通过降解c-Myc来调节结直肠癌的发生。MAGI3基因缺失与预后不良相关，是结直肠癌患者氟嘧啶类化疗的潜在预测生物标志物。（生物谷 Bioon.com）参考文献 Haibo Wang et al. E3 ubiquitin ligase MAGI3 degrades c-Myc and acts as a predictor for chemotherapy response in colorectal cancer. Mol Cancer. 2022 Jul 22;21(1):151. doi: 10.1186/s12943-022-01622-9.

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