SUMO1 | small ubiquitin_like modifier protein 1
- Known as:
- SUMO1 | small ubiquitin_like modifier protein 1
- Catalog number:
- AS08308
- Product Quantity:
- 1.5 mg
- Category:
- -
- Supplier:
- Agris
- Gene target:
- SUMO1 | small ubiquitin_like modifier protein 1
Related genes to: SUMO1 | small ubiquitin_like modifier protein 1
- Gene:
- SUMO1 NIH gene
- Name:
- small ubiquitin like modifier 1
- Previous symbol:
- UBL1
- Synonyms:
- PIC1, GMP1, SMT3C, SUMO-1, SMT3H3, OFC10
- Chromosome:
- 2q33.1
- Locus Type:
- gene with protein product
- Date approved:
- 1996-06-04
- Date modifiied:
- 2019-02-18
Related products to: SUMO1 | small ubiquitin_like modifier protein 1
Related articles to: SUMO1 | small ubiquitin_like modifier protein 1
- The transcription factor ZEB2 has been implicated in cardiovascular disease, but its role and post-translational regulation in cardiac fibroblast-to-myofibroblast transition (FMT) and fibrosis after myocardial infarction (MI) are not fully understood. ZEB2 protein expression was significantly increased in infarcted murine hearts, activated cardiac fibroblasts, and human fibrotic myocardium. Myofibroblast-specific ZEB2 knockout alleviates cardiac dysfunction and adverse remodeling post-MI. Mechanistically, SENP1 regulated SUMO-1 modification of ZEB2 at K462, K479, K611, and K774. Reconstituting ZEB2-deficient systems with wild-type ZEB2 (ZEB2-WT) restored pathological fibrosis and FMT, whereas the SUMOylation-deficient mutant (ZEB2-4KR) conferred cardioprotective effects. ZEB2 SUMOylation activated the pro-fibrotic PI3K/AKT-mTORC1 signaling pathway. ZEB2-4KR weakens CtBP1 binding and enhances ZEB2 occupancy at the Nr4a1 promoter. Importantly, Nr4a1 knockdown abolished the protective effects of ZEB2-4KR. These findings identify SUMO-1 modification of ZEB2 as a central driver and molecular switch of pathological cardiac remodeling after MI and suggest that targeting ZEB2 SUMOylation may represent a promising therapeutic strategy. - Source: PubMed
Publication date: 2026/08/06
Wang YilinCheng ShaopengChen HongyuYang ZhihaoWu XiaotingZong QiuyanWang JianingJiang YiYu YanrongChen HaoXue YunxingZhao QianwenYang JieWang Dongjin - Endoplasmic reticulum (ER) stress is a key driver of diabetic cardiomyopathy (DCM), but its upstream regulators are incompletely defined. The transcription factor DACH1 is genetically linked to diabetes and cardiovascular risk, yet its role in the diabetic heart is unknown. - Source: PubMed
Publication date: 2026/08/08
Lin JieLiu NaLi BoWang YiLi CongyeYin YueMa HengYu LuZhou Jie - Post-translational modifications, particularly SUMOylation, plays a crucial role in α-synuclein (α-syn) aggregation, a key pathological feature of Parkinson's disease (PD). Curcumin, a natural polyphenol, has shown neuroprotective potential, but its effects on SUMOylation-related signaling in PD remain unclear. - Source: PubMed
Publication date: 2026/07/21
Li YaoZhu ZhuangZhang Kezhong - Although bovine herpesvirus 1 (BoHV-1) causes massive losses of cattle, the transition from mucosal replication to neuroinvasion remains poorly understood. Using a controlled calf model, we integrated quantitative virology and transcriptomics to map its pathogenesis and define the role of promyelocytic leukemia protein (PML). Calves inoculated intranasally and ocularly (1.4 × 10 plaque-forming units/head) were sampled daily (1-14 days post-infection, dpi) for glycoprotein B (gB) qPCR. Tissues were analyzed at 4 and 14 dpi to measure viral DNA via gB-specific qPCR, and for mRNA-seq of trigeminal ganglia (TG). Shedding peaked at 3-6 dpi, being highest in nasal samples, lower in ocular samples, and substantially lower in rectal samples, and declined by 10-14 dpi. At 4 dpi, among the tissues sampled, the tonsils exhibited the highest viral burden. TG exhibited low viral levels at 4 dpi, although they remained detectable at 14 dpi, indicating neuroinvasion. The TG program shifted from early proteostasis priming (4 dpi) to immune/extracellular matrix activation with synaptic repression (14 dpi). In MDBK/Vero cells, IFN-α resulted in higher bovine PML (bPML) levels and enlarged PML nuclear bodies (PML-NBs), reducing very early viral DNA levels, whereas BoHV-1 disrupted PML-NB integrity. The different bPML isoforms exerted different effects on viral infection. STRING analysis revealed a conserved PML-SUMO1-UBE2I-DAXX-SP100 core. These findings delineate the mucosal-to-neuronal trajectory, establish PML as both an effector and viral target in complementary systems, and identify SUMO/ubiquitin-linked proteostasis as a tractable target for antiviral intervention.IMPORTANCEAlthough bovine herpesvirus 1 (BoHV-1) remains a major challenge to cattle health, the early transition from mucosal replication to trigeminal neuroinvasion has not been clearly mapped in natural-host calves. By integrating daily shedding kinetics, tissue viral DNA profiling, and time-resolved trigeminal ganglion transcriptomics, we delineate when and how BoHV-1 reaches the sensory neurons. Promyelocytic leukemia protein (PML) is identified as a key intrinsic antiviral factor that is upregulated by IFN-α and restricts very early viral genome accumulation, while viral BoHV-1-encoded infected cell protein 0 actively dismantles PML nuclear bodies. The discovery of opposing isoform-specific PML functions and a conserved PML-SUMO proteostasis hub provides mechanistic insight into BoHV-1 immune evasion. These findings refine our understanding of the mucosal-to-neuronal trajectory of infection and highlight proteostasis-linked antiviral pathways as promising targets for intervention. - Source: PubMed
Publication date: 2026/07/23
Wang YongJin HuanWang FanyuCheng JingCao MengyaoZhou LinyiLiu WenxiaoLi Yongqing - Primary sclerosing cholangitis (PSC) is an immune-mediated cholestatic liver disease. Its molecular etiology remains poorly defined, hindering the development of mechanism-based diagnostics and therapies. Therefore, this study aimed to identify key molecular drivers and causal biomarkers of PSC by integrating transcriptomics, machine learning, and genetic causal inference. - Source: PubMed
Publication date: 2026/03/20
Cheng PengfeiQiang YuanmingSun YiboDuan BinweiOuyang YaboLi Guangming