Ask about this productRelated genes to: TNFRSF25 Blocking Peptide
- Gene:
- TNFRSF25 NIH gene
- Name:
- TNF receptor superfamily member 25
- Previous symbol:
- TNFRSF12
- Synonyms:
- DR3, TRAMP, WSL-1, LARD, WSL-LR, DDR3, TR3, APO-3
- Chromosome:
- 1p36.31
- Locus Type:
- gene with protein product
- Date approved:
- 1998-12-04
- Date modifiied:
- 2016-10-05
Related products to: TNFRSF25 Blocking Peptide
Related articles to: TNFRSF25 Blocking Peptide
- Hidradenitis suppurativa (HS) is a chronic inflammatory disorder that presents with both cutaneous manifestations and extracutaneous comorbidities. Current treatment options include antibiotics and biologics; however, treatment failure is common and often surgical intervention is required for acceptable control. Anti-TL1A therapies have recently gained attention in HS treatment due to their ability to inhibit the TL1A/DR3 axis, a key signaling pathway driving immune cell activity and fibrosis. Participant recruitment for the phase 2b trial (NCT06956235) assessing the efficacy of anti-TL1A therapy tulisokibart in moderate-to severe HS was reported on 1 December, 2025 to be completed. This review aims to explore the potential links between the TL1A and HS by synthesizing immune mechanisms of HS pathogenesis with existing data of the TL1A/DR3 axis in immune pathways. A discussion highlighting the potential for anti-TL1A therapies as a class that simultaneously addresses fibrosis and comorbidities of HS is also presented, and future directions to address knowledge gaps are also proposed. - Source: PubMed
Publication date: 2026/04/22
Sia JulingLee BernettOon Hazel H - Bladder cancer (BLCA) is clinically heterogeneous, and conventional staging does not fully capture individual risk. Ribosome biogenesis (RiBi) is implicated in cancer, but its prognostic relevance in BLCA is not well defined. - Source: PubMed
Publication date: 2026/04/16
Luo GuangyueWang WeiboTai SupengYan LeiLuo HailangChang YifanYang LexingYan JunyiZhou JunLiang Chaozhao - Maternal immune activation (MIA) contributes to neurodevelopmental deficits in offspring, yet the prenatal mechanisms remain elusive. Here, using a mouse MIA model induced by prenatal exposure to Toxoplasma gondii soluble tachyzoite antigen (STAg), we reveal that maternal gut dysbiosis, characterized by increased Firmicutes and Actinobacteria, drives offspring behavioral deficits. This dysbiosis disrupts intestinal barrier integrity and induces metabolic and inflammatory dysregulation, characterized by elevated M1 macrophages and IL-6, alongside a pronounced accumulation of the glycerophospholipid metabolite 1-oleoyl-2-myristoyl-sn-glycero-3-phosphocholine (OMPC), resulting in adverse outcomes including placental inflammation, fetal neuroinflammation, and behavioral abnormalities in offspring. Mechanistically, OMPC binds to Tnfrsf25 on macrophages, activating JAK1/STAT3/IL-6 signaling. Crucially, maternal probiotic supplementation with Lactobacillus rhamnosus GG (LGG) restores gut-immune homeostasis, attenuates placental inflammation and fetal neuroinflammation, and rescues offspring behavioral impairments. Collectively, our findings define OMPC/JAK1/STAT3/IL-6 signaling as a pathogenic hub in MIA and nominate LGG as a prenatal prophylactic strategy to mitigate neurodevelopmental disorders. - Source: PubMed
Publication date: 2026/03/31
Chang HaoZhu XinyiShen ChunxiangXu XuejunNi YangyueZhang YuYan JumingXue JingyaoLi ChiQin QiHai KexinHou MinZhou ZikaiJi MinjunXu Zhipeng - Hearing loss is a prevalent sensory condition that affects the ability to perceive sounds. Hair cells play a vital role in hearing by converting mechanical sound vibrations into electrical signals that are transmitted to the brain. In humans, if damaged, these specialized sensory cells do not regenerate, leading to reduced sensitivity to sound, difficulty understanding speech, and deafness. The incidence of hearing loss increases with age, but it can also occur earlier due to genetic predisposition or environmental factors such as exposure to noise or ototoxic medications. Epigenetic mechanisms play a significant role in age-related hearing loss (ARHL) by regulating gene expression without changing the underlying DNA sequence. Aberrant DNA methylation patterns have been linked to ARHL. In this study, by performing an epigenome-wide association study in a cohort of 30 ARHL patients, we found a correlation between a specific CpG site methylation level proximal to the gene, with an impaired hearing threshold. Interestingly, absence in mice cause ARHL, severe hair cell depletion, and degeneration of nerve fibers. Taking together these results suggests a crucial role of expression in hearing maintenance. - Source: PubMed
Publication date: 2026/03/26
Roche Marie ValerieTang Pei-CiaoYan DeniseDe Marchena Michelle RoseRobayo Maria CamilaAbad ClemerGuo YanGong FengWalz KatherinaLiu Xue Zhong - Rheumatoid arthritis (RA) and major depressive disorder (MDD) are interconnected conditions with a growing incidence, yet the mechanism that links them remains uncertain. This research focused on identifying the overlapping genes and pathogenic processes of RA and MDD via bioinformatics and National Health and Nutrition Examination Survey (NHANES) validation. - Source: PubMed
Publication date: 2026/02/11
Deng ChuyuHe ZhenhuaZhu Xiaofeng