TNFSF12 is a cytokine that belongs to the tumor necrosis factor (TNF) ligand family. This protein is a ligand for the FN14_TWEAKR receptor. This cytokine has overlapping signaling functions with TNF,
- Known as:
- TNFSF12 a cytokine belongs tumor necrosis factor (TNF) ligand family. protein a ligand FN14_TWEAKR receptor. cytokine overlapping signaling functions TNF,
- Catalog number:
- 25-364
- Product Quantity:
- 0.05 mg
- Category:
- -
- Supplier:
- Prosci
- Gene target:
- TNFSF12 cytokine that belongs the tumor necrosis factor (TNF) ligand family. This protein for FN14_TWEAKR receptor. has overlapping signaling functions with TNF
Related genes to: TNFSF12 is a cytokine that belongs to the tumor necrosis factor (TNF) ligand family. This protein is a ligand for the FN14_TWEAKR receptor. This cytokine has overlapping signaling functions with TNF,
- Gene:
- BTF3P11 NIH gene
- Name:
- basic transcription factor 3 pseudogene 11
- Previous symbol:
- BTF3L1
- Synonyms:
- HUMBTFB, TNFRSF11B, OPG, OCIF
- Chromosome:
- 13q22.3
- Locus Type:
- pseudogene
- Date approved:
- 1997-12-12
- Date modifiied:
- 2016-10-05
- Gene:
- C1QL1 NIH gene
- Name:
- complement C1q like 1
- Previous symbol:
- -
- Synonyms:
- CRF, C1QRF, C1QTNF14, CTRP14
- Chromosome:
- 17q21.31
- Locus Type:
- gene with protein product
- Date approved:
- 2004-05-06
- Date modifiied:
- 2018-07-16
- Gene:
- C1QL2 NIH gene
- Name:
- complement C1q like 2
- Previous symbol:
- -
- Synonyms:
- CTRP10, C1QTNF10
- Chromosome:
- 2q14.2
- Locus Type:
- gene with protein product
- Date approved:
- 2004-05-18
- Date modifiied:
- 2016-07-04
- Gene:
- C1QL3 NIH gene
- Name:
- complement C1q like 3
- Previous symbol:
- -
- Synonyms:
- K100, C1ql, C1QTNF13, CTRP13
- Chromosome:
- 10p13
- Locus Type:
- gene with protein product
- Date approved:
- 2004-05-19
- Date modifiied:
- 2018-11-15
- Gene:
- C1QL4 NIH gene
- Name:
- complement C1q like 4
- Previous symbol:
- -
- Synonyms:
- C1QTNF11, CTRP11
- Chromosome:
- 12q13.12
- Locus Type:
- gene with protein product
- Date approved:
- 2005-03-22
- Date modifiied:
- 2016-07-04
Related products to: TNFSF12 is a cytokine that belongs to the tumor necrosis factor (TNF) ligand family. This protein is a ligand for the FN14_TWEAKR receptor. This cytokine has overlapping signaling functions with TNF,
Related articles to: TNFSF12 is a cytokine that belongs to the tumor necrosis factor (TNF) ligand family. This protein is a ligand for the FN14_TWEAKR receptor. This cytokine has overlapping signaling functions with TNF,
- To assess genetic associations thatsupporta plausible causal interpretation of the obesity-chronic apical periodontitis (CAP) relationship, and to screen mediators including inflammatory cytokines, immune cell profiles and gut microbiota. - Source: PubMed
Publication date: 2026/09/29
Zhu LijingYang Xuechao - Intestinal barrier dysfunction and mucus layer abnormalities are central features of inflammatory bowel disease, yet the epithelial mechanisms regulating goblet cell function remain incompletely understood. The TWEAK/Fn14 pathway is involved in intestinal inflammation, but its role in small intestinal epithelial responses, particularly in goblet cells, has not been fully clarified. In this study, we investigated TWEAK/Fn14 signaling using mouse small intestinal epithelial organoids. Fn14 was expressed in MUC2-positive cells in intestinal tissue, with staining preferentially observed toward the mucin-facing region. Fn14 staining was also observed in small intestinal epithelial organoids. TWEAK stimulation increased mRNA expression by approximately 1.56-fold and reduced mRNA expression to approximately 66% of control, without markedly affecting epithelial proliferation or stem cell markers. TWEAK did not significantly alter the PAS-positive mucin area or AB-PAS-defined mucin composition, whereas PGM34 staining showed a non-significant tendency to increase. TNF treatment reproduced some of the TWEAK-associated changes, including reduced mRNA expression and alterations in mucin-associated parameters, suggesting that TNF may contribute to some of the epithelial responses associated with TWEAK treatment. Treatment with an anti-TNF neutralizing antibody modified several TWEAK-associated responses, including changes in epithelial-associated gene expression and mucin-associated staining parameters. These findings suggest that TWEAK treatment is associated with goblet cell-related mucin responses in mouse small intestinal epithelial organoids, with possible involvement of TNF signaling. - Source: PubMed
Publication date: 2026/08/26
Tamaki ShunKono MasayukiArikawa SakuraHigashi YuiMaekawa TatsunoriHara YusukeTsujimoto TaizoKawakami FumitakaImai MotokiKurosaki YoshifumiNaito ShokichiIshii NaohitoIchikawa TakafumiKawashima Rei - Mitochondrial dysfunction is an important cause of sarcopenia, and TWEAK/Fn14, as one of the major muscle wasting cytokines, its role in the development of sarcopenia by regulating mitochondrial biogenesis remains unclear. Expression of TWEAK in old and young mice was both detected. TWEAK was silenced in C2C12 myocytes using lentiviral vectors. Immunofluorescence, western blot, real-time polymerase chain reaction (RT-PCR), and ELISA were enrolled to analyze the effects of TWEAK on myotube size, mitochondrial content, mitochondrial ROS, and inflammatory factors. Additionally, aged mice received two injections of AAV9 vectors at 15 and 17 months of age. Upon reaching 18 months of age, the effects of TWEAK knockdown on grip strength, muscle mass, and gastrocnemius muscle indices were evaluated. TWEAK/Fn14 expression was significantly increased in old mice (p < 0.001). Compared with young controls, old mice exhibited a significant decrease in grip strength (p < 0.001) and a significant increase in lean mass (p < 0.05), whereas no significant difference was observed in fat content. In DEX-treated C2C12 myotubes, TWEAK knockdown significantly increased myotube diameter, enhanced ATP content and mitochondrial quantity, upregulated protein expression of SIRT1, PGC-1α, and p-AMPK, and inhibited mitochondrial ROS, Ca levels, p-p38 expression, and the secretion of inflammatory cytokines (TNF-α, IL-1β, IL-6, and iNOS). In aged mice, TWEAK knockdown did not significantly alter forelimb grip strength or lean mass, but significantly increased fat mass (p < 0.05). Mechanistically, TWEAK knockdown promoted AMPK signaling, inhibited p38 MAPK activation, enhanced mitochondrial biogenesis, and reduced serum levels of IL-1β, IL-6, and iNOS (p < 0.05), whereas serum TNF-α levels showed no significant difference. TWEAK knockdown attenuates age-related skeletal muscle mass loss and improves mitochondrial biogenesis in skeletal muscle, accompanied by modulated inflammatory factor release and altered AMPK-p38 MAPK signaling activity. However, no significant improvement in forelimb grip strength was observed in the in vivo experiment. These findings indicate that TWEAK suppression may represent a promising strategy for preserving muscle mass and metabolic homeostasis during aging, though its capacity to fully restore functional capacity requires further investigation. - Source: PubMed
Publication date: 2026/08/14
Maimaitiwusiman ZhuoyaXuekelati SaiyareWang AnyanAiriken NadilaXu YanbinGuo ShukeYang YiningWang Hongmei - Sarcopenia is characterized by the progressive loss of skeletal muscle mass and strength, accompanied by impaired regenerative capacity. This study examined age-related changes in skeletal muscle regeneration and the associated expression of tumor necrosis factor-like weak inducer of apoptosis (TWEAK) and myogenin (MyoG). Male C57BL/6 mice aged 3, 13, and 23 months were subjected to barium chloride (BaCl)-induced tibialis anterior muscle injury. In parallel, C2C12 cells were exposed to repeated low-dose hydrogen peroxide (HO) to induce senescence-associated changes under oxidative stress, and the effect of the TWEAK inhibitor L524 was evaluated. Muscle mass and grip strength showed age-dependent declines. Following BaCl injury, MyoD expression was induced similarly across age groups, whereas MyoG and embryonic myosin heavy chain expression significantly decreased with advancing age. TWEAK expression increased in injured muscle with age, while p-4E-BP1 showed no clear age-dependent change. In C2C12 cells, repeated HO exposure at 100 μM, which maintained cell viability above 90%, induced senescence-associated changes, reduced myotube formation, increased TWEAK expression, and decreased MyoG expression, whereas treatment with the TWEAK inhibitor L524 attenuated the HO-associated reduction in MyoG expression. Collectively, these findings suggest that TWEAK signaling may be associated with oxidative stress and age-related impairments in muscle regeneration. - Source: PubMed
Publication date: 2026/08/25
Kim Jin-HwaKim Hyun-TaeKim Jeong-WonJeong Ji-SooLee Su-HaKim Kwan-HooKim Na-YoungKim Young-HunKo Je-WonKim Tae-Won - BACKGROUNDElucidating immune signals through well-defined cohorts of pediatric acute pancreatitis (AP) and chronic pancreatitis (CP) patients is critical. This study aimed to evaluate plasma chemokine and cytokine levels in pediatric participants with CP, compared with AP and healthy controls (HCs), to identify unique biomarkers of CP.METHODSIndividuals were identified from a prospectively collected pediatric cohort (n = 146). Immunoproteins (n = 247) were measured using the NULISAseq platform on samples from individuals with CP (n = 71), AP (n = 55), and HCs (n = 20).RESULTSThe measured analytes showed separation among the 3 groups (R2 = 0.13, P < 0.001). In the CP group, TRANCE, TWEAK, FLT-1, HGF, and TRAIL were increased when compared with HC and AP patients (FDR-corrected P <0.05). A multivariable logistic regression model including all 5 proteins provided an AUC of 0.94 (0.93-0.96) for differentiating samples from CP versus AP or HC samples. In the AP group, CRP, IL-6, CD3E, ENRAGE, and MIF were elevated compared with HCs, while FGF-2, TAFA-5, IL-33, TRANCE, and CXCL12 were downregulated in the same acute time period (FDR-corrected P < 0.05). In the 21 patients with AP for whom follow-up samples were obtained, there was a notable decrease in sequential expression of IL-6 and CRP over 12 months and increased expression of CCL25, TAFA-5, and TRANCE proteins. Additionally, TRANCE was expressed on CP pancreatic tissue.CONCLUSIONSTRANCE was increased in pediatric patients with CP and decreased in those with AP during a flare. Future studies are needed to investigate the role of TRANCE and other analytes in the pathogenesis of CP. - Source: PubMed
Publication date: 2026/08/24
Farrell Peter RLee BomiAhmed FaizanMoreno-Fernandez Maria EDixit AjayGurria Juan PabloOllberding Nicholas JDuan QingGarlapally VineetChristian PhoebeHusain Sohail ZAbu-El-Haija Maisam