Ask about this productRelated genes to: SESN1 antibody
- Gene:
- SESN1 NIH gene
- Name:
- sestrin 1
- Previous symbol:
- -
- Synonyms:
- SEST1, PA26
- Chromosome:
- 6q21
- Locus Type:
- gene with protein product
- Date approved:
- 2003-09-03
- Date modifiied:
- 2014-11-19
Related products to: SESN1 antibody
Related articles to: SESN1 antibody
- RNA viruses, major pathogens of humans and animals, are responsible for numerous inflammatory diseases. Commonly, mild RNA virus infection fails to trigger inflammatory diseases due to host immune homeostasis. However, severe RNA virus infection destroys immune homeostasis and causes hyperinflammation. The detail mechanism is still unclear. Here, we reported that SESN1 acts as a critical negative regulator of mitochondrial antiviral signaling protein (MAVS), a central hub protein in RNA-triggered innate immune response, by potentiating MAVS autophagic degradation to repress innate immune response. Upon low dose RNA virus infection, SESN1 level was decreased at infection early stage and was rebounded at late stage, which restrained SESN1-mediated MAVS degradation to clear virus at early stage and enhanced MAVS degradation to prevent excessive cytokines production at late stage. Whereas, SESN1 level was continuously impaired after high dose RNA virus infection, which caused robust cytokines production. Notably, we observed that the expression of SESN1 was markedly downregulated and negatively correlated with cytokine levels in patients with severe influenza. Replenishment of SESN1 effectively inhibited cytokines production in the Human Primary Bronchial/Tracheal Epithelial Cells infected with Influenza A virus PR8 and peripheral blood mononuclear cells of patients with severe influenza. Mechanistically, SESN1 interacted with MAVS and enhanced MAVS autophagic degradation via SQSTM1. Together, these findings revealed SESN1 was an important factor to regulate host innate immune response. - Source: PubMed
Publication date: 2026/08/26
Liu QianghuiChen PeiranHe ChunyanQiu ZuochengZhang YuboWang JiaXu LingxiaoXu YongPan Mingyu - ObjectiveSystemic lupus erythematosus is associated with increased cardiovascular morbidity, even in the absence of overt clinical disease. Sestrin-1 is a stress-responsive antioxidant protein implicated in oxidative homeostasis and cardiovascular protection. This study aimed to evaluate serum Sestrin-1 levels in patients with systemic lupus erythematosus and examine their relationship with subclinical cardiovascular findings.MethodsIn this controlled cross-sectional study, 60 patients with systemic lupus erythematosus and 60 age-matched healthy controls underwent clinical assessment, laboratory testing, 12-lead electrocardiography, transthoracic echocardiography, and carotid intima-media thickness measurement. Serum Sestrin-1 was measured by enzyme-linked immunosorbent assay (ELISA). Between-group comparisons used parametric or nonparametric tests according to data distribution. Within the systemic lupus erythematosus cohort, correlations between Sestrin-1 and disease activity (Systemic Lupus Erythematosus Disease Activity Index), as well as cardiovascular parameters, were assessed. An exploratory multivariable logistic regression model including Sestrin-1, left atrial diameter, corrected QT interval, age, and sex was constructed to identify variables associated with case status.ResultsSerum Sestrin-1 levels were significantly lower in patients with systemic lupus erythematosus than in controls (9.99 ± 2.01 vs. 17.79 ± 5.11 ng/mL; p < 0.001). Patients with systemic lupus erythematosus had a significantly longer corrected QT interval (429.65 ± 32.42 vs. 376.26 ± 33.41 ms; p < 0.001). In the exploratory multivariable logistic regression analysis, lower Sestrin-1 (per 1ng/mL increase, odds ratio 0.63; 95% confidence interval: 0.54-0.75; p < 0.001), larger left atrial diameter (per 1 mm increase, odds ratio 1.13; 95% confidence interval: 1.06-1.22; p < 0.001)), and longer corrected QT interval (per 1ms increase, odds ratio 1.03; 95% confidence interval: 1.02-1.05; p < 0.001) were independently associated with systemic lupus erythematosus status.ConclusionPatients with systemic lupus erythematosus exhibit markedly reduced serum Sestrin-1 levels together with subclinical cardiovascular abnormalities. The inverse relationship between Sestrin-1 and left atrial diameter suggests a possible link between reduced antioxidant defense and early atrial remodeling in systemic lupus erythematosus. Sestrin-1 may represent a promising candidate biomarker for subclinical cardiovascular involvement in patients with systemic lupus erythematosus; however, prospective studies are needed to confirm its clinical utility. - Source: PubMed
Publication date: 2026/07/27
Ucar CahitCelik MustafaGoktepe Mevlut HakanYildizgoren Mustafa TurgutIlanbey BilalKucuk Adem - Breast cancer is the most common cancer in women and the second most frequent cancer worldwide. Changes in miRNA levels are associated with various diseases, including cancer, making them ideal non-invasive biomarkers for diagnosis, prognosis, and treatment. Bioinformatics advancements have enabled the prediction of miRNAs and their target genes. This study aimed to analyze the miR-15 family (miR-15a, miR-15b, miR-16-1, miR-16-2, miR-195, and miR-497) to predict their target genes and evaluate their role in breast cancer progression. - Source: PubMed
Publication date: 2026/05/29
Alizadeh MahdiSalimi Mahdieh - Diarrhetic shellfish toxins (DSTs) are the most widely distributed algal toxins in marine environment. Although DSTs exhibit diverse toxic effects, their neurotoxicity on marine fish remains poorly understood. Swimming behavior of fish is a sensitive indicator of neurotoxicity, and locomotor ability is of vital importance for their survival. This study systematically investigated the impact of exposure to the DSTs-producing dinoflagellate Prorocentrum lima (2 × 10 cells/L) on swimming behavior in the marine model fish Oryzias melastigma and explored potential neurotoxicity-related mechanisms. After 96 h of exposure, the fish showed significant reductions in average swimming speed, acceleration, and total distance, along with increased frozen events and altered swimming trajectories. Correspondingly, brain tissue damage was observed, accompanied by marked decreases in neurotransmitter levels, including acetylcholine, dopamine, and serotonin. Transcriptomic analysis suggested potential disturbances in neurotransmitter system, calcium signaling, and myelination following DSTs exposure. The altered expressions of irak4, il-1b, il-12, atr, sesn1, and ppm1d pointed to the activation of oxidative stress and inflammatory responses, which likely exacerbate neural damage. This structural compromise was further supported by the inhibition of ECM-receptor interaction and focal adhesion pathway. Crucially, detected brain DSTs and molecular docking suggested that Slco1d1 may be involved in DSTs-associated brain toxicity, although its role in mediating DSTs across the blood-brain barrier remains to be verified. Collectively, these findings indicate that DSTs-producing algal exposure may impair swimming behavior and neural function in marine medaka, potentially involving neurotransmitter dysregulation, calcium signaling disturbance, myelination-related changes, and brain tissue injury. - Source: PubMed
Publication date: 2026/06/10
Chen Zi-MinLi Mei-QiJiang Jing-XuanMo Yan-HangLi Da-WeiLi Hong-YeYang Wei-Dong - Atherosclerosis (AS) is a major contributor to cardiovascular and cerebrovascular disorders. Although aerobic exercise is widely regarded as a beneficial non-pharmacological therapy, the specific molecular basis for its protective effects remains incompletely defined. Sestrin proteins are a conserved family of proteins, and sestrin 1 (SESN1) has been associated with both AS pathologies and exercise-related physiological effects. Clarifying how SESN1 contributes to exercise-induced protective effects may enhance understanding of exercise-based cardiovascular rehabilitation. - Source: PubMed
Publication date: 2026/06/03
Sun YunfengWu Yawei