RIPK1 Antibody
- Known as:
- RIPK1 Antibody
- Catalog number:
- 5389
- Product Quantity:
- 0.1 mg
- Category:
- -
- Supplier:
- Prosci
- Gene target:
- RIPK1 Antibody
Related genes to: RIPK1 Antibody
- 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
Related articles to: RIPK1 Antibody
- 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 - A series of new compounds was designed and synthesized based on the pronounced anticancer activities of the thiazole ring and hydrazone groups against breast cancer cells. IR, H NMR, C NMR (decoupled and APT), F NMR, 2D NMR (HSQC), HRMS and elemental analysis data were used to confirm the structures of the compounds. Cytotoxicity was assessed by the MTT assay, while immunoperoxidase staining was used to examine the distribution of caspase-3, BAX, Bcl2, cytochrome c, Ki-67, RIPK1, RIPK3, and MLKL in breast cancer cell lines (M4A4 and MCF-7). Compounds 4b, 4c, 4d, 4g, 4h, and 4l were the most effective derivatives in the series against MCF-7 and M4A4 cancer cells, with IC values of 51-106 μM and 12.87-100 μM, respectively. Molecular docking and molecular dynamics (MD) simulations were performed to elucidate the interactions between compound 4l, which has the best BAX: Bcl2 ratio, and the BAX and Bcl2 proteins. In addition, molecular docking and MD simulations showed that compound 4l stably binds within the Bcl2 BH3-binding groove, maintaining key interactions with ASP108, TYR105, and ARG143 during the 300 ns simulation. The RMSD remained below 2.5 Å after equilibration, supporting the structural stability of the complex. - Source: PubMed
Publication date: 2026/06/15
Tok FatihEnsarioğlu Hilal KabadayıBaşoğlu FaikaBecer EdaKıyak NadireVatansever Hafize Seda - Necroptosis plays a significant role in the pathogenesis of systemic lupus erythematosus (SLE) and lupus nephritis (LN). Nonetheless, the therapeutic potential of necroptosis inhibition in these conditions remains unclear. - Source: PubMed
Publication date: 2026/06/19
Chen MingWan LiyanWang MinhuiLiang JunyuKe YiniJiang MengdiLiu JingCao Heng