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更新于：2025-05-07

SUMO2

更新于：2025-05-07

基本信息

别名

HSMT3、Sentrin-2、small ubiquitin like modifier 2

+ [8]

简介

Ubiquitin-like protein that can be covalently attached to proteins as a monomer or as a lysine-linked polymer. Covalent attachment via an isopeptide bond to its substrates requires prior activation by the E1 complex SAE1-SAE2 and linkage to the E2 enzyme UBE2I, and can be promoted by an E3 ligase such as PIAS1-4, RANBP2, CBX4 or ZNF451 (PubMed:26524494). This post-translational modification on lysine residues of proteins plays a crucial role in a number of cellular processes such as nuclear transport, DNA replication and repair, mitosis and signal transduction. Polymeric SUMO2 chains are also susceptible to polyubiquitination which functions as a signal for proteasomal degradation of modified proteins (PubMed:18408734, PubMed:18538659, PubMed:21965678, PubMed:9556629). Plays a role in the regulation of sumoylation status of SETX (PubMed:24105744).

关联

100 项与 SUMO2 相关的临床结果

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100 项与 SUMO2 相关的转化医学

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0 项与 SUMO2 相关的专利（医药）

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470

项与 SUMO2 相关的文献（医药）

2025-12-01·Molecular Biology Reports

mir-188‐5p emerges as an oncomir to promote chronic myeloid leukemia via upregulation of BUB3 and SUMO2

Article

作者: Petrovic, Nina ; Misir, Sema ; Akidan, Osman

BACKGROUNDChronic myeloid leukemia (CML) is an aggressive malignancy originating from hematopoietic stem cells. miRNAs play a role in physiological and developmental processes, including cellular proliferation, apoptosis, angiogenesis, and differentiation, and in CML's prognosis, diagnosis, and treatment. This study aimed to investigate the function and possible mechanisms of action of miR-188-5p in the development and progression of chronic myeloid leukemia.METHODS AND RESULTSmiRNA expression profiles were obtained from the GSE90773 dataset in the Gene Expression Omnibus (GEO). GEO2R was used to identify differentially expressed miRNAs. miRNET, miRDB, CancerSEA, GeneMANIA, and BioGRID databases were applied to assess the biological function of miRNA and target molecules in CML. RT-PCR performed validation analyses of miRNA and target molecules in CML. To determine the power of miR-188-5p expression levels to distinguish patients with CML from control, the ROC analysis was performed. miR-188-5p is significantly increased in K-562 cells, and overexpression of miR-188-5p was associated with clinicopathological features. miR-188-5p showed significantly higher AUC values (AUC = 1.0, p = 0.0001). The cut-off of miR-188-5p was 6.74. miRDB and mirNET predicted BUB3 and SUMO2 as a potential target gene of miR-188-5p. Additionally, increased expression of BUB3 and SUMO2 was observed in the K-562 cell. Bub3 is implicated in apoptosis and the cell cycle, whereas Sumo2 protein sumoylation and DNA binding are believed to contribute to catabolic processes.CONCLUSIONSOur results suggest that miR-188-5p acts as an oncomiRNA in CML pathogenesis and may be a promising therapeutic target for CML.

2025-03-01·Alzheimer's & Dementia

Genetic and pharmacologic enhancement of SUMO2 conjugation prevents and reverses cognitive impairment and synaptotoxicity in a preclinical model of Alzheimer's disease

Article

作者: Arancio, Ottavio ; Fraser, Paul E. ; Acquarone, Erica ; Yamauchi, Hiroto ; Matsuzaki, Shinsuke ; Fioriti, Luana ; Argyrousi, Elentina K. ; Katayama, Taiichi ; Wijesekara, Nadeeja ; Martucci, Annacarla ; Takamura, Hironori ; Satoh, Kanayo ; Han, Kyung ; Staniszewski, Agnieszka ; Orsini, Franca

AbstractINTRODUCTIONAmyloid beta oligomers (Aβos) are toxic to synapses and key to the progression of Alzheimer's disease (AD) and amyloid pathology, representing a target for therapeutic strategies.METHODSAmyloid and small ubiquitin modifier 2 (SUMO2) transgenics were analyzed by electrophysiology and behavioral testing. A recombinant analogue of SUMO2, SBT02, was generated and assessed for brain penetration and the ability to mitigate amyloid pathology.RESULTSElevated SUMO2 expression prevents cognitive and synaptic impairment in a mouse model of AD amyloid pathology. Systemic administration of SBT02 resulted in high brain bioavailability and prophylactically halted the progression of AD‐associated deficits. SBT02 also restored cognition and synaptic function in late‐stage amyloid load. Mechanistically, SUMO2 and SBT02 do not alter amyloid processing or clearance and mitigate synaptotoxicity in the presence of high amyloid loads.DISCUSSIONSBT02 is a promising therapeutic strategy to counteract and reverse the toxic effects of Aβos in AD.Highlights

Genetic overexpression of human SUMO2 prevents the long‐term potentiation (LTP) impairments and cognitive deficits in amyloid precursor protein (APP) transgenics without affecting amyloid pathology.

A recombinant analogue of human SUMO2, termed SBT02, when administered systemically, displays high brain bioavailability and has no adverse effects at high doses.

Prophylactic treatment of APP transgenics with SBT02 prior to the development of amyloid pathology results in the prevention of synaptic and behavioral dysfunction.

SBT02 also reverses pre‐existing LTP and cognitive impairments when administered to APP transgenics with advanced and severe pathology.

SBT02 has no impact on amyloid pathology, indicating a mechanism of action on synaptic resistance to Aβ toxicity.

2025-02-01·Cancer Letters

Bone marrow stromal cells protect myeloma cells from ferroptosis through GPX4 deSUMOylation

Article

作者: Wang, Yixuan ; Li, Tiantian ; Cheng, Hao ; Hu, Meilin ; Zhao, Haifeng ; Wang, Sheng ; Wang, Jingjing ; Peng, Ziyi ; Guo, Jing ; Yang, Xudan ; Wang, Lijuan ; Li, Xin ; Jia, Linchuang ; Jiang, Hongmei ; Xie, Ying ; Liu, Zhiqiang ; Wang, Jingya ; Wang, Mengqi ; Li, Qian

Bone marrow stromal cells (BMSCs) are vital for preventing chemotherapy induced apoptosis of multiple myeloma (MM), but roles and machinery in other forms of cell death have not been well elucidated. Here, using an in vitro BMSC-MM interacting model, we observed BMSCs protected MM cells from labile iron pool (LIP) and reactive oxygen species (ROS) triggered ferroptosis by elevating glutathione peroxidase 4 (GPX4). Mechanistically, direct interaction with BMSCs upregulated the expression of SUMO-specific protease 3 (SENP3) in MM cells through CD40/CD40L signaling pathway, and SENP3 de-conjugated SUMO2 at lysine 75 residue to stabilize GPX4 protein, thereby consuming ROS to obviate ferroptosis in MM cells from the Vk∗MYC mouse model, as well as in CD138⁺B220^- cells separated from the Cd40l^fl/fl;Prx1^Cre/+ mice (CD40-CKO) and Sumo2 knock out (SUMO2-KO) mice. Using the NOD-scid IL2Rgamma^null (NSG) mouse based xenograft model and intra-bone MM growth model, we validated that target SENP3 enhanced the killing effect of GPX4 inhibitor RSL3, thereby reduced tumor burden, prolonged survival of mice, and alleviated bone disruption of mice bearing MM tumors. Our study deciphers the mechanism of BMSCs preventing MM cells from spontaneous ferroptosis, and clarifies the therapeutic potential of non-apoptosis strategies in managing refractory or relapsed MM patients.

项与 SUMO2 相关的新闻（医药）

2022-07-27

·生物谷

J Clin Invest: KRAS基因突变是胰腺癌细胞外小泡淋巴管生成的重要启动子

该研究提供了对癌症淋巴管生成的机制洞察，具有开发生物标记物和RAS途径疗法的潜力。胰腺癌是最致命的胃肠道恶性肿瘤，是癌症相关死亡的第四大原因，五年生存率最低，仅为11%。由于缺乏筛查方法和早期症状的缺乏，胰腺癌最常在晚期被发现-当时几乎没有可用的治疗选择。主要的组织学类型是胰腺导管腺癌(PDAC)，90%以上的病例携带KRAS基因突变作为分子标志。作为胰腺癌的驱动基因，KRAS基因改变促进了胰腺上皮异型增生、胰腺上皮内瘤变和胰腺粘液瘤的发生发展。直到最近，由于设计特定抑制剂的结构困难，KRAS突变被认为是不可药物的靶点。图片来源: https://doi.org/10.1172/JCI161454. 近日，来自罗马尼亚的研究者们在J Clin Invest杂志上发表了题为“KRAS mutations as essential promoters of lymphangiogenesis via extracellular vesicles in pancreatic cancer”的文章，该研究提供了对癌症淋巴管生成的机制洞察，具有开发生物标记物和RAS途径疗法的潜力。柯尔斯滕鼠肉瘤病毒(KRAS)基因突变存在于90%以上的胰腺导管腺癌(PDAC)中。KrasG12D是最常见的改变，促进癌前病变，并与更具侵袭性的表型相关。这些肿瘤具有瘤内淋巴管网络增多和频繁的淋巴转移。罗、李等人探讨了KrasG12D突变与PDAC淋巴管生成的关系。作者使用体外和体内模型和一种优雅的机制方法来描述促进淋巴管生成的另一种途径。KrasG12D通过SAE1和SUMO2的激活诱导异源核糖核蛋白A1(HnRNPA1)的SUMO化。 SUMOylated hnRNPA1被负载到细胞外小泡(EVS)中，并被人内皮淋巴细胞(HLEC)内化。此外，SUMOylated hnRNPA1通过稳定PROX1的mRNA，促进淋巴管生成和LN转移。 KrasG12D诱导PDAC淋巴管生成的可能机制图片来源: https://doi.org/10.1172/JCI161454. 综上所述，本研究揭示了KrasG12D PDAC中肿瘤诱导淋巴管发育和早期LN转移的分子机制。作者发现KrasG12D蛋白是血管内皮生长因子-C非依赖性诱导淋巴管生成的重要因素。在机制上，KrasG12D在激活依赖于SAE1的hnRNPA1的SUMO化和随后的EV负载方面发挥了作用，从而进一步诱导了HLEC中PROX1的激活。（生物谷 Bioon.com）参考文献 Radu Pirlog et al. KRAS mutations as essential promoters of lymphangiogenesis via extracellular vesicles in pancreatic cancer. J Clin Invest. 2022 Jul 15;132(14):e161454. doi: 10.1172/JCI161454.

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