SUMO2

Last update 08 May 2025

Basic Info

Synonyms

HSMT3, Sentrin-2, small ubiquitin like modifier 2

+ [8]

Introduction

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).

100 Clinical Results associated with SUMO2

100 Translational Medicine associated with SUMO2

0 Patents (Medical) associated with SUMO2

470

Literatures (Medical) associated with SUMO2

01 Dec 2025·Molecular Biology Reports

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

Article

Author: 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.

01 Mar 2025·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

Author: 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.

01 Feb 2025·Cancer Letters

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

Article

Author: 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.

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SUMO2

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