RIPK1 Antibody (C_term) Blocking Peptide
- Known as:
- RIPK1 Antibody (C_term) Blocking Peptide
- Catalog number:
- BP7817b
- Product Quantity:
- 0.1 mg
- Category:
- -
- Supplier:
- Abgen
- Gene target:
- RIPK1 Antibody (C_term) Blocking Peptide
Related genes to: RIPK1 Antibody (C_term) Blocking Peptide
- Gene:
- RIPK1 NIH gene
- Name:
- receptor interacting serine/threonine kinase 1
- Previous symbol:
- -
- Synonyms:
- RIP
- Chromosome:
- 6p25.2
- Locus Type:
- gene with protein product
- Date approved:
- 1999-05-07
- Date modifiied:
- 2015-11-17
Related products to: RIPK1 Antibody (C_term) Blocking Peptide
Related articles to: RIPK1 Antibody (C_term) Blocking Peptide
- Integrin-linked kinase (ILK) maintains endothelial homeostasis by supporting endothelial nitric oxide synthase activity and restraining vascular inflammation. Although endothelial ILK loss is linked to vascular and cardiac disease, the mechanisms driving progression remain unclear. We hypothesized that extracellular vesicles (EVs) released by ILK-deficient endothelial cells propagate endothelial activation and cardiac dysfunction. In endothelial-specific ILK conditional knockout mice, ILK loss induced rapid endothelial activation, marked by increased iNOS, VCAM-1 and ICAM-1, followed by perivascular macrophage accumulation and chronic cardiac inflammation. In vitro, ILK-deficient endothelial cells exhibited barrier dysfunction, NF-κB activation and increased chemokine production. EVs derived from ILK deficient cells were enriched in pro-inflammatory cargo, including receptor-interacting protein kinase 1 (RIPK1), and transferred the activation phenotype to naïve endothelial cells. RIPK1 inhibition in recipient cells or RIPK1 silencing in donor cells abolished EV-induced activation, thereby confirming a necessary role for RIPK1. Endothelial ILK-deficient mice also exhibited increased circulating EVs enriched in endothelial activation markers and RIPK1. Transfer of these EVs to wild type mice induced coronary endothelial activation, macrophage recruitment, microvascular remodelling, cardiac fibrosis, and ventricular dysfunction mimicking the phenotype of the donor mice. RIPK1-dependent inflammatory effects were similarly observed with EVs from atherosclerotic ApoE/ mice and patients with coronary artery disease. These findings reveal an ILK-RIPK1 EV signalling axis that propagates vascular inflammation and promotes cardiac dysfunction, establishing a conserved pathogenic mechanism operative in experimental models and in human coronary artery atherosclerosis. - Source: PubMed
Cook-Calvete AlbertoDelgado-Marín MaríaJorquera Ortega SaraMoreta SilviaCastro-Pinto MercedesLópez-Menendez JoséRodríguez-Fernandez BlancaGarcía-García JuliaZaragoza CarlosSaura Marta - Tumor necrosis factor (TNF) is a key driver of intestinal epithelial inflammation. The baculoviral inhibitor of apoptosis protein repeat-containing 3 (BIRC3) gene encodes the cellular inhibitor of apoptosis protein 2 (cIAP2), a known regulator of TNF signaling. Although genetic variants in components of the TNF signaling pathway have been reported, no human BIRC3 variants have been previously identified. - Source: PubMed
Publication date: 2026/06/23
Li QiNambu RyusukeYaqiang HuShen XiangArgmann CarmenGuan ReiJanssen ErinLe Voyer TomWarner NeilYu Daniel DGuo JingLong KelvinOuahed JodieField MichaelCollen LaurenBibus JonasIllig DavidRohlfs MeinoYu ZiqiYang ShaohongLi WenjuanPlatt Craig DComella Phillip HJordan DanielSuárez-Fariñas MayteAlosaimi Mohammed FPeters Lauren ARosain JeremieFieschi ClairePuel AnneHsieh Elena W YNaito TakeoZeng ZhiyangRodríguez-Belvís Marta VelascoPalomino LauraKüster PeterLi DalinKlein ChristophSnapper Scott BCasanova Jean-LaurentGeha RaifHoffenberg EdwardMcGovern Dermot P BSchadt EricKotlarz DanielLi DaliMuise Aleixo M - T cell responses are regulated by co-stimulatory and inhibitory signalling pathways, driven by receptors and their ligands designated as immune checkpoints. These receptors belong either to the immunoglobulin superfamily or the tumour necrosis factor receptor (TNFR) superfamily. Despite their crucial role in enhancing T effector cell activity, the molecular mechanisms triggered by TNFR co-stimulatory receptors, particularly their integration into the T cell receptor (TCR) signalling network, remain incompletely characterised. The receptor Fas is classically recognised as the prototypical TNFR death receptor due to the presence of an intracellular death domain (DD). While best known for its ability to trigger cell death, Fas has also been involved in non-death functions, including T cell co-stimulation. Despite its key role in dictating T cell fate, the molecular mechanisms underlying its TCR co-stimulatory receptor function have not been fully elucidated. We show here that Fas constitutively concentrates in plasma membrane domains at the immune synapse where it can be activated by antigen-presenting cell (APC) membrane-anchored FasL. This proximity to the TCR signalling molecules allows Fas, in a DD-independent manner, to lower the TCR activation threshold thereby enhancing the number of activated cells. Additionally, Fas triggers a DD-dependent signalling cascade composed of FADD, caspase-8 and RIPK1, ultimately leading to TAK1 activation. TAK1 in turn initiates gene-activating signalling pathways essential for an optimal Fas co-stimulatory response. Moreover, we identified the catalytic activity of caspase-8 as a tipping point in Fas signalling during TCR co-stimulation. Indeed, inhibiting caspase 8 not only prevents cell death but also promotes T cell co-stimulation by favouring RIPK1-dependent signalling. Altogether, our findings reveal a complex mechanism by which Fas integrates at multiple levels of the TCR spatial organization and signalling network, synergising with TCR signalling to achieve full T cell activation. - Source: PubMed
Publication date: 2026/06/20
Miloro GiorgiaGagnoux-Palacios LaurentHuault SébastienLoubat AgnèsFormisano AnthonyGuo Xiao-JunJenei ViktóriaKoncz GáborHe Hai-TaoHueber Anne-OdileRossin Aurélie - Non-alcoholic fatty liver disease (NAFLD) is currently the most common chronic liver disease worldwide. Necroptosis is a controlled, programmed form of cell death, with its core comprising a highly conserved signaling pathway that primarily involves key proteins, including Receptor-interacting protein kinase-1 (RIPK1), RIPK3, and Mixed lineage kinase domain-like protein (MLKL). Diosgenin (DG), classified as a steroidal saponin, exhibits anti-inflammatory, immune-regulating, and lipid-lowering properties, demonstrating efficacy in ameliorating dyslipidemia across multiple metabolic pathologies. However, the exact signaling pathways involved in improving NAFLD and preventing liver damage remain unclear. In our study, the data showed that the administration of diosgenin effectively mitigated hepatic damage and excessive lipid deposition in the high-fat diet (HFD)-induced rat model. Meanwhile, it also significantly downregulates Tumor necrosis factor-α (TNF-α), Tumor necrosis factor receptor-1 (TNFR1), and Tumor necrosis factor receptor-associated death domain protein (TRADD), inhibits upstream signaling of the necroptosis pathway, and suppresses necroptosis by reducing RIPK1, RIPK3, and MLKL phosphorylation. DG decreases cell damage and inhibits the expression of necroptosis-related genes in free fatty acids (FFAs)-induced HepG2 cells, which is consistent with the results of in vivo experiments. We inhibited and overexpressed RIPK1 in vitro for further research. Inhibition of RIPK1 enhances the effect of DG on NAFLD, while overexpression of RIPK1 partially reverses its beneficial effect. In addition, to test whether DG acts independently of upstream TNF-α, we introduced exogenous recombinant TNF-α to amplify upstream signals. In conclusion, DG has a favorable reduction effect on NAFLD through the RIPK1-dependent necroptosis signaling pathway. Also, this study offers further data and a theoretical basis for the use of natural medicines to improve NAFLD. - Source: PubMed
Publication date: 2026/06/20
Qi MuxiYin GuoliangWang ShujunXie NaZhang XinYu WenfeiMeng DechengWang LinyaSun YuqingLiu HongshuaiJiang WenyingLiu DiZhang Fengxia - Vascular cognitive impairment (VCI) is a common form of dementia associated with cerebrovascular dysfunction and chronic inflammation. Impaired cerebral perfusion is a result of atherosclerotic plaque build-up in the medium and large arteries in the brain and is exacerbated by numerous inflammatory triggers, including aging, high blood pressure, high cholesterol, and smoking. Previously, we demonstrated that receptor-interacting protein 1 kinase (RIPK1) promotes the progression of aortic atherosclerosis and NFκB activation in mice, and that atherosclerotic vascular disease was decreased by therapeutically inhibiting RIPK1 with antisense oligonucleotides. Given the relationship between atherosclerosis and cognitive impairment, we hypothesize that RIPK1 also contributes to the development of cerebrovascular disease and neuroinflammation in a mouse model of hyperlipidemia. Male and female Apoe were fed a chow or Western diet (WD) for 16 weeks and subsequently treated for an additional 8 weeks with either scramble (control) or anti-RIPK1 antisense oligonucleotides (ASO) to systemically knockdown RIPK1 expression (RIPK1). WD feeding induced significant carotid atherosclerotic lesion burden and reduced cerebral blood flow compared to chow-fed mice. These vascular changes were associated with impaired spatial learning and memory, reduced hippocampal vascularity, and altered expression of neurovascular and inflammatory markers. Systemic RIPK1 silencing significantly reduced carotid artery lesion size, restored arterial stiffness and blood flow in the brain. Furthermore, treatment with RIPK1 preserved vascularity in the hippocampus, restored blood flow in the brain and prevented the impairment in spatial learning and memory. Overall, our study identifies RIPK1 as a mediator of hyperlipidemia-induced cerebrovascular dysfunction and suggests that targeting RIPK1 may represent a therapeutic approach to limit cognitive impairment. - Source: PubMed
Publication date: 2026/06/20
Salazar-Leon JonathanFreitas-Andrade MoisesGuadarrama-Perez VioletaSolari SerenaHudak AbagaelStotts CameronSimon NancyGeoffrion MichèleMurray SueSlack RuthLacoste BaptisteRayner Katey J