Ask about this productRelated genes to: TWEAK protein
- Gene:
- TNFSF12 NIH gene
- Name:
- TNF superfamily member 12
- Previous symbol:
- -
- Synonyms:
- TWEAK, DR3LG, APO3L
- Chromosome:
- 17p13.1
- Locus Type:
- gene with protein product
- Date approved:
- 1998-12-04
- Date modifiied:
- 2019-04-23
Related products to: TWEAK protein
Related articles to: TWEAK protein
- Erectile dysfunction (ED) is increasingly prevalent worldwide, arising from complex interactions between genetic susceptibility and environmental exposure. Real-world exposure involves complex chemical mixtures that may induce synergistic toxicity, which traditional methods struggle to elucidate. This study integrates multi-omics data with reverse network toxicology to systematically identify causal molecular targets and environmental pollutants underlying ED risk, thereby clarifying their mechanisms. - Source: PubMed
Publication date: 2026/04/02
Yang QingtaoYu QiLi WeiWei XiShi JiangQiao JunGu ChangshiSun FaLi Tao - Cardio-cerebrovascular diseases (CCVDs), notably stroke and coronary heart disease, represent the leading causes of mortality and disability worldwide. The intricate bidirectional feedback between the brain and heart in brain-heart syndrome (BHS) exacerbates clinical outcomes and imposes a significant economic burden on patients. The cytokine tumor necrosis factor-like apoptosis weak inducer (TWEAK) and its receptor fibroblast growth factor-inducible 14 (Fn14) are overexpressed in cerebral injury and cardiac dysfunction. Elevated levels of TWEAK and Fn14 contribute to the development of various brain diseases, including blood-brain barrier damage, brain edema, neuroinflammation, neuronal apoptosis, and neurodegeneration. Additionally, the TWEAK-Fn14 axis is implicated in numerous pathophysiological events in the heart, such as cardiomyocyte proliferation, inflammation, apoptosis, hypertrophy, fibrosis, contractile function disruption, and ventricular dilatation. Given its significant contributions to CCVDs, the TWEAK-Fn14 axis has also emerged as a promising therapeutic target for BHS. In this review, the critical roles of TWEAK-Fn14 in CCVDs and its potential interplay between the brain-heart axis in BHS were updated and discussed, which shed a new light on co-treatment of brain and heart and brain-heart syndrome. - Source: PubMed
Publication date: 2026/04/01
Fei QinglinChang JunJiang TingcanGuan GuoqiangLiang YujuanCheng CuicuiXiao GuangxuGuo QiuyanFan GuanweiZhu YanLyu Ming - Thyroid carcinoma is characterized by significant heterogeneity and immune evasion, in which myeloid cells play a pivotal role in tumor microenvironment (TME) remodeling. However, the key regulatory genes and their underlying mechanisms are not yet fully elucidated. - Source: PubMed
Yu JunjieLi JingjingGao ShengnanWang LilanQiao Hong - Joint use of multiple molecular layers can be useful to prioritize targets for mechanistic studies. Application of coronary disease in large populations is an emerging field. - Source: PubMed
Publication date: 2026/04/02
El-Sabawi BassimHuang XiaoningLin PhillipAnwar Mohammad YaserBetti MichaelKim NamjuPerry Andrew SPerera B Lakshitha AGajjar PriyaColangelo Laura AAmancherla KaushikSheng QuanhuZhao ShilinStolze LindsayFarber-Eger EricLandman Joshua MMiller Patricia ELiu Gabrielle YDas SumanWells Quinn STerry James GLloyd-Jones DonaldDas SaumyaKhan Sadiya SNorth Kari EBelow JenniferNayor MatthewKalhan RaviCarr John JeffreyGamazon Eric RShah Ravi V - Oxidative stress (OS) is increasingly implicated in benign prostatic hyperplasia (BPH), yet the underlying cellular programs remain unclear. We integrated multi-omics and machine learning to identify OS-associated biomarkers and to characterize OS-linked stromal states, with targeted experimental validation. - Source: PubMed
Publication date: 2026/04/01
Chen JieBai JingxingChen BoHuang YinLi JinzeChen ZeyuRan BiaoWei QiangAi JianzhongLiu LiangrenCao Dehong