TWEAK
- Known as:
- TWEAK
- Catalog number:
- BC-082
- Product Quantity:
- 10 ug
- Category:
- -
- Supplier:
- kamyia
- Gene target:
- TWEAK
Related genes to: TWEAK
- 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
Related articles to: TWEAK
- The immunopathogenesis of clade IIb monkeypox virus (MPXV) infection and its relationship with clinical severity remain poorly defined. We characterized cytokine responses in acute and convalescent mpox to delineate inflammatory profiles. - Source: PubMed
Publication date: 2026/07/23
Byrne JoanneSaini GurvinGarcia-Leon AlejandroAlalwan DanaLanday AlanNguyen Liem Binh LuongSavinelli StefanoO'Broin CathalHorgan MaryKelly ChristineCotter AoifeSadlier Corinnade Barra EoghanO'Halloran Jane AGautier VirginieMallon Patrick W GFeeney Eoin R - To explore the causal relationships between human inflammatory proteins and hypertrophic scars (HS) and keloids. This study was conducted based on bidirectional two-sample Mendelian randomization (MR) analysis. Data of human inflammatory proteins, HS, and keloids were acquired from genome-wide association study database. The inverse variance weighted (IVW) method was adopted to evaluate the causal relationships between 91 kinds of human inflammatory proteins and HS and keloids, i.e., a forward MR analysis. For the above associations, Cochran's Q test was used to assess heterogeneity, MR-Egger regression and MR-PRESSO outlier tests were performed to evaluate horizontal pleiotropy, and the leave-one-out method was applied to analyze the robustness of the results. The IVW method was also used to evaluate whether there was a reverse causal relationship between HS, keloids and inflammatory proteins screened out by aforementioned forward MR analysis. CD6, leukemia inhibitory factor (LIF), tumor necrosis factor ligand superfamily member 12 (TNFSF12), programmed death-ligand 1 (PD-L1), interleukin-17C (IL-17C), LIF receptor (LIFR), osteoprotegerin (OPG), and fibroblast growth factor 23 (FGF23) had significant causal relationships with HS (with s of 1.365, 0.506, 1.567, 1.683, 0.621, 1.375, 0.623, and 0.553, respectively, 95% s of 1.100-1.693, 0.289-0.887, 1.081-2.273, 1.090-2.599, 0.408-0.947, 1.025-1.845, 0.402-0.966, and 0.315-0.971, respectively, <0.05). Among them, CD6, TNFSF12, PD-L1, and LIFR were risk factors for HS, while LIF, IL-17C, OPG, and FGF23 were protective factors for HS. CD5, IL-10 receptor subunit alpha (IL-10RA), IL-5, LIF, and OPG had significant causal relationships with keloids (with s of 0.744, 1.303, 0.686, 0.603, and 0.715, respectively, 95% s of 0.573-0.965, 1.024-1.660, 0.472-0.996, 0.431-0.842, and 0.553-0.924, respectively, <0.05). Among them, IL-10RA was a risk factor for keloids, whereas CD5, IL-5, LIF, and OPG were protective factors for keloids. No significant heterogeneity or horizontal pleiotropy was observed in the above associations (>0.05), and the robustness of the results was not driven by any single nucleotide polymorphism. Significant reverse causal relationships existed between HS and TNFSF12 and LIFR of the 8 inflammatory proteins which had significant causal relationships with HS screened out by aforementioned forward MR analysis (with s of 0.972 and 0.968, respectively, 95% s of 0.949-0.997 and 0.942-0.994, respectively, <0.05). No reverse causal relationship was found between keloids and the 5 inflammatory proteins which had significant causal relationships with keloids screened out by aforementioned forward MR analysis (>0.05). CD6, TNFSF12, PD-L1, and LIFR may increase the risk of HS, while LIF, IL-17C, OPG, and FGF23 may decrease the risk of HS. IL-10RA may increase the risk of keloids, while CD5, IL-5, LIF, and OPG may decrease the risk of keloids. - Source: PubMed
Wang S SXiao KXiao H THan D WZhang JWang LLi Y C - Tumor-associated macrophages (TAMs) play a crucial role in colorectal cancer (CRC) metastasis, particularly in the establishment of the liver metastatic niche. TAMs facilitate metastasis by enabling epithelial-mesenchymal transition (EMT) and suppressing anti-tumor immunity. While their roles in primary tumors have been extensively investigated, their functions at metastatic sites remain poorly understood. In this study, we analyzed the single-cell RNA sequencing data from 46 CRC patients, encompassing 402,972 cells, to identify macrophage subsets associated with liver metastasis. A distinct population of APOC1 IFI30 TAMs was identified and found to be significantly enriched in metastatic liver lesions. Compared to primary tumors (PT), the number of APOC1 IFI30 TAMs significantly increased at liver metastatic sites after CRC cells metastasized to the liver. We employed spatial transcriptomics to validate the above conclusions. These TAMs exhibited significantly enhanced immunosuppressive capacity and cholesterol synthesis metabolism. Further investigation showed that TAMs within metastatic niches reprogram the mevalonate pathway to enhance cholesterol synthesis, characterized by upregulation of key genes such as HMGCR and ACAT1/2. These TAMs act on surrounding tumor cells by secreting cholesterol and cytokines such as TNFSF12, TGFB1, MIF and LGALS9, thereby enhancing tumor adhesion and proliferation and creating an immunosuppressive microenvironment to continuously support tumor growth. Our findings provided new insights into the complex interactions among TAMs, immune cells, and tumor cells within CRC metastatic microenvironment, highlighting potential therapeutic targets to disrupt TAMs-mediated immune evasion and metastatic progression. - Source: PubMed
Publication date: 2026/07/11
Cai ZheyouChen YibingCui LeiYao JineQiao JianghuaSun WeihongLiu HaishengYang LinhaoYang ZhuangLiu QuentinHou BenxinZou ZhengzhiLai Dongming - The causal links between metabolites, inflammatory cytokines, and Primary Sclerosing Cholangitis (PSC) remain elusive. This study used Mendelian Randomization (MR) to elucidate these mechanistic pathways. - Source: PubMed
Publication date: 2026/06/23
Liu HuiZhong ZhiweiNing Shoubin - Polycystic ovary syndrome (PCOS) is the most common endocrine disorder in reproductive-aged women, characterized by aberrant follicular development and a dysregulated ovarian microenvironment. The roles of intercellular communication, particularly between ovarian endothelial cells and granulosa cells, remain poorly understood. The TWEAK (TNF-like weak inducer of apoptosis)-Fn14 (fibroblast growth factor-inducible 14) axis, implicated in apoptosis and cellular stress, represents a potential but unexplored pathway in PCOS. - Source: PubMed
Publication date: 2026/06/15
Chen FangxueGu TingWu Juanhong