Ask about this productRelated genes to: SENP1 antibody
- Gene:
- SENP1 NIH gene
- Name:
- SUMO specific peptidase 1
- Previous symbol:
- -
- Synonyms:
- -
- Chromosome:
- 12q13.11
- Locus Type:
- gene with protein product
- Date approved:
- 2004-02-20
- Date modifiied:
- 2018-02-23
Related products to: SENP1 antibody
Related articles to: SENP1 antibody
- To explore the regulatory role of SENP1 in ferroptosis of differentiated thyroid cancer cells and its molecular mechanism. - Source: PubMed
Zhu FeifeiYan NaYang JiwenChen XiaoleiWang Yingying - Colonic immune homeostasis is critically maintained by regulatory T (Treg) cells. Here, we identify SUMO-specific peptidase 1 (SENP1) as an important regulator of colonic Treg function and intestinal immune homeostasis. Treg-specific Senp1 deletion does not impair thymic Treg development, but selectively disrupts the homeostasis of colonic Treg subset without affecting Treg maintenance in other peripheral tissues. Mechanistically, SENP1 deficiency reduces CD25 expression on Tregs, blunting IL-2 responsiveness and compromising their expansion and survival. This is associated with a selective reduction in the proportion of tissue-adapted Gata3 Tregs and accumulation of CD25 precursor-like Tregs in the intestinal lamina propria. Senp1 depletion also downregulates core effector Treg signature genes including Gata3, Klrg1, and Il1rl1, correlating with dysregulated Th2 response control. Single-cell RNA sequencing analysis reveals transcriptional alterations consistent with impaired colonic Treg tissue adaptation after SENP1 ablation. Functionally, with adoptive transfer experiments we found that Senp1-deficient Tregs show impaired accumulation in vivo and are associated with weaker control of pathogenic T cell expansion in the colon. Consistently, Treg-specific Senp1-deficient mice display heightened susceptibility to DSS-induced colitis, highlighting a critical role of SENP1 in sustaining functional Treg programs and limiting pathogenic intestinal inflammation. - Source: PubMed
Publication date: 2026/05/16
Hao YanyunLiu HongzhiLiang QiuliFan QiujuWang TianshiCheng Jinke - Intervertebral disc degeneration (IDD) is a leading cause of global disability. This study aimed to systematically investigate the role of SUMOylation in the pathogenesis of IDD through integrated transcriptomic analysis. - Source: PubMed
Publication date: 2026/05/11
Xu ZhaoqiangHao KunZhang TianyiYang XuPeng ShuaiYang GuoweiZhao JieZhao YachaoWu Dongjin - Hepatocellular carcinoma (HCC) is a global crisis. Long noncoding RNAs (lncRNAs) are anticipated to be significant players in the pathogenesis of HCC in a multitude of ways, including tumor progression, proliferation, invasion, metastasis, and recurrence. To limit the progression of hepatocarcinogenesis, we employ a new treatment regimen that delivers lncRNA SRHC via polymer nanoparticles. A total of 100 mice were divided into five different groups. The initial group served as a control and received saline injections. On the other hand, the pathological-control group received weekly N-Nitrosodiethylamine (DEN) injections for 16 weeks. The remaining three groups received injections of polymer nanoparticles (NPs), long noncoding RNA SRHC alone, or conjugated NPs, respectively, once a week for four weeks, starting in the 12th week after DEN injection. After 16 weeks, the animals were euthanized, and liver specimens and blood samples were collected for biochemical, molecular, and pathological evaluations. Using nanoconjugates containing the lncRNA SRHC significantly improved tumor-associated biomarkers and histopathology compared with the pathological-control group. Furthermore, the expression of SENP1 and PCNA was downregulated. In conclusion, SRHC-conjugated nanoparticles are more likely to be considered a cutting-edge HCC treatment protocol. - Source: PubMed
Publication date: 2026/05/09
Elkramani NabilaElzallat MohamedMohammed Dina MostafaAbdelLatif AhmedAboushousha TarekEl-Ahwany Eman - Subarachnoid hemorrhage (SAH) is a critical condition in neurosurgery, and the severity of early brain injury (EBI) plays a pivotal role in determining patient outcomes. Recent studies have demonstrated that neuronal pyroptosis occurs following SAH, aggravating neuroinflammatory damage and severely affecting prognosis. Small ubiquitin-like modifier (SUMO)-specific protease 1 (Senp1), a member of the SUMO protease family, is known to be involved in the regulation of neuroinflammation. However, whether Senp1 also modulates neuronal pyroptosis to influence neuroinflammation after SAH remains unclear. - Source: PubMed
Publication date: 2026/05/02
Ma YinruiLong HaiboXiong HanCui ShizhenZhuang YiminWei HaotianHe ZhaohuiTan Jiahe