Ask about this productRelated genes to: TNFSF4 antibody
- Gene:
- TNFSF4 NIH gene
- Name:
- TNF superfamily member 4
- Previous symbol:
- TXGP1
- Synonyms:
- OX-40L, gp34, CD252
- Chromosome:
- 1q25.1
- Locus Type:
- gene with protein product
- Date approved:
- 1993-12-15
- Date modifiied:
- 2017-03-02
Related products to: TNFSF4 antibody
Related articles to: TNFSF4 antibody
- Acute kidney injury (AKI) often progresses to chronic kidney disease (CKD) characterized by renal fibrosis, yet the regulatory mechanisms driving this transition remain elusive. Here, it is demonstrated that tumor necrosis factor superfamily member 4 (TNFSF4/OX40L) significantly upregulates in proximal tubular cells (PTCs) from patients with CKD and in murine models of AKI-CKD transition induced by unilateral ischemia-reperfusion injury (uIRI) or repeated low-dose cisplatin. Elevated TNFSF4 levels correlates positively with the severity of tubulointerstitial injury and negatively with estimated glomerular filtration rate. Functionally, proximal tubule-specific deletion of Tnfsf4 markedly ameliorates tubular damage, renal inflammation and interstitial fibrosis in both AKI-CKD models. Furthermore, anti-TNFSF4 monoclonal antibody exerts its therapeutic effects in AKI-CKD mice suffering from uIRI. Conversely, overexpression of TNFSF4 exacerbates pro-fibrotic responses in PTCs under TGF-β1 or chronic hypoxia conditions. Mechanistically, immunoprecipitation-mass spectrometry identifies an interaction between TNFSF4 and glycogen synthase kinase-3α (GSK-3α). TNFSF4 blocks synaptotagmin-like protein 4 (SYTL4)-mediated ubiquitination of GSK-3α, prolongs its half-life, and sustains profibrotic signaling, effects reversed by GSK-3α knockdown. Collectively, these results uncover a previously unrecognized TNFSF4-GSK-3α axis as a key proximal tubule-intrinsic driver of AKI-CKD progression, and propose targeting this pathway as a promising therapeutic strategy to mitigate renal fibrosis and halt AKI-CKD transition. - Source: PubMed
Publication date: 2026/05/06
Yang KexinZhang LeiXiong ZiyiLu YingyingZhang ShuminLiu YifeiZhang LeiCai JuanTang ChengyuanLiu YuDeng TuoSun LinLiu FuyouDuan ShaobinXiao Li - The etiopathogenesis of juvenile systemic lupus erythematosus (JSLE), a complex and complicated illness, is unknown. Genetic, environmental, and dysregulated immune system responses are all thought to contribute to the disease's etiology. Important immunological molecules that regulate different immune cells and are associated with autoimmune disorders are TNFSF4 and IKZF1. Thus, our purpose was to discover if TNFSF4 and IKZF1 mutations left the Egyptian population genetically predisposed to SLE. - Source: PubMed
Publication date: 2026/03/19
Attia Zeinab RAmshawee Ahmed MHasan Ahmed FlayyihHussein Dalia TawfeekAbd El Azeem Rania AZedan Mohamed MMutawi Thuraya MEl-Beltagy Nanis SEl Basuni Mohamed A - In hepatocellular carcinoma (HCC), molecularly targeted therapies have been the major focus of recent research. In this study, we evaluated the clinical and biological roles of tumor necrosis factor superfamily 4 (TNFSF4), an inflammatory cytokine, as a therapeutic target in HCC. - Source: PubMed
Publication date: 2026/02/14
Hosoda KiyotakaMasuda TakaakiSaito HideyukiKoike KensukeAndo YukiAbe TadashiHashimoto MasahiroNakano YusukeDairaku KatsushiHirose KosukeMatsumoto ChihiroIkehara TomohikoOfuchi TakashiKawata KotoOmachi KazukiTobo TaroTsuda YasuoOtsu HajimeYonemura YusukeShimizu AkiraSoejima YujiMimori Koshi - Dendritic cells (DCs) facilitate the maintenance of immunological tolerance in the steady state. We report that transcription factor Etv3 is preferentially expressed in mature DCs, including tissue-derived migratory DCs (migDCs), and facilitates their homeostatic maturation and CCR7-dependent migration. Mice with global or DC-specific deletion of Etv3 manifested the expansion of CD25 regulatory T (T) cells, spontaneous activation of conventional T cells, and multiorgan T cell infiltration. Etv3 deficiency exacerbated TLR7-driven systemic lupus erythematosus (SLE)-like disease, supporting the reported genetic association of human with SLE. Etv3-deficient migDCs up-regulated multiple costimulatory molecules, including OX40 ligand (OX40L/TNFSF4), whose blockade partially rescued the T cell abnormalities. These results identify Etv3 as an essential regulator of the tolerogenic function of DCs and implicate it in the regulation of human autoimmunity. - Source: PubMed
Publication date: 2026/02/12
Adams Nicholas MMartinez-Krams DanielEsteva EduardoRa Ai CAlexiou Allegra IliadiJin HuaYun Tae JinTellaoui Rayan SleimanMudianto TennyVollmer EmilyNovikova EkaterinaTan YanjunHuntley WilliamKrichevsky OlegDolgalev IgorIzmirly PeterBuyon Jill PMoreira Andre LLund Amanda WReizis Boris - Immunotherapy targeting immune checkpoint proteins (ICPs) has transformed cancer care, yet current treatments focus on a narrow set of inhibitory ICPs and benefit only a subset of patients. The co-stimulatory pair OX40-OX40L, implicated in inflammation and autoimmunity, also plays roles in cancer immunity. We previously showed that high OX40L mRNA expression in melanoma correlates with favorable prognosis and improved responses to PD-1 blockade. However, the protein-level expression and functions of OX40L in melanoma remain poorly defined. - Source: PubMed
Publication date: 2026/01/23
Feldman SusannaDa'ana BaseemOfek NonaElkis LilianaPollak-Moseri AdiRiklin-Nahmias EmmanuelaMendlovic SoniaAvraham AyeletLeibowitz Raya