RIPK1 ELISA kit
- Known as:
- RIPK1 Enzyme-linked immunosorbent assay test reagent
- Catalog number:
- DL-RIPK1-Hu
- Product Quantity:
- 96T
- Category:
- Elisa Kits
- Supplier:
- WDSTD
- Gene target:
- RIPK1 ELISA kit
Related genes to: RIPK1 ELISA kit
- 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
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- Ischemia-reperfusion injury (IRI) greatly impairs lung transplantation (LTx) outcomes, with no effective treatments. Although existing studies have confirmed that cell death and inflammation responses are critical in LTx-IRI, the specific cell death profiles of various parenchymal and inflammatory cells remain to be elucidated. - Source: PubMed
Publication date: 2026/07/04
Li JinshengMa XingjieHuang JinghaoYu YifanLou ZhilingLiang FuxiangHu XiaolongFang QiuyuWang YongchaoLiu MingyaoLu YunbiWu Ming - Liver aging is characterized by chronic inflammation and metabolic dysfunction that drive progression of metabolic dysfunction-associated steatotic liver disease (MASLD). Necroptosis, a pro-inflammatory form of cell death via the Receptor-Interacting serine/threonine-Protein Kinase 1 (RIPK1)-RIPK3-Mixed Lineage kinase domain Like pseudokinase (MLKL) pathway, is activated in aging livers, and systemic inhibition of this pathway reduces hepatic inflammation and pathology. The cell type-specific role of necroptosis in liver aging, however, is unclear. Notably, RIPK3 is suppressed in hepatocytes under metabolic disease, suggesting necroptosis independent functions for MLKL. Here, we show that MLKL is elevated in aged hepatocytes and drives liver aging via a non-necroptotic mechanism. Using hepatocyte-specific MLKL-overexpressing mice (MLKL), we find that MLKL overexpression does not induce necroptosis but instead promotes cellular senescence, evidenced by increased p16INK4a and p21WAF1/Cip1 and elevated senescence associated secretory phenotype (SASP). Mechanistically, MLKL induces hepatocyte mitochondrial dysfunction, with impaired respiration, altered mitochondrial dynamics, and increased reactive oxygen species, implicating oxidative stress as a contributing mechanism. This mitochondrial stress is associated with enhanced release of pro-inflammatory extracellular vesicles (EVs) and induction of senescence in hepatocytes and non-parenchymal cells. While hepatocytes contribute substantially to total senescent burden by abundance, macrophages emerge as a senescence-enriched population, indicating amplification of senescence through non-cell-autonomous signaling. Collectively, these findings reveal a non-lethal, non-necroptotic function of hepatocyte MLKL in promoting liver inflammaging via mitochondrial dysfunction and paracrine senescence signaling, identifying MLKL as a regulator of hepatic aging and a potential therapeutic target in age-associated liver disease. - Source: PubMed
Mohammed SabiraJiang ChaoPennington TravisBhaskaran ShyleshOhene-Marfo PhoebeKneuper Kara FGeorgescu ConstantinPitts KamilleTran AlbertPeng ZongkaiSingh AmitYang ZhiboLi TiangangHannafon BethanyHouchen CourtneyWren Jonathan DYabluchanskiy AndriyGalvan VeronicaAhsan NagibKinter MichaelLewis Tommy LDeepa Sathyaseelan S - Understanding the complex connections between cellular mechanisms is crucial for developing effective cancer treatments. In this study, new Schiff base derivative triazine compounds (5-8) were synthesized and structurally characterized using various spectroscopic techniques to investigate their cellular and gene-protein-level effects in lung cancer and to develop anticancer activity strategies. The cytotoxic activities of compounds were evaluated against A549 and MRC-5 cell lines using the WST-8 assay. Moreover, cellular death mechanisms in lung cancer were investigated using methods such as qRT-PCR, ELISA, membrane array, and Flow cytometry. In lung cancer cells, compounds 5 (58.24%) and 6 (59.08%) were mildly effective in terms of cell viability, and these two compounds exhibited cytotoxic activity at a dose of 50 µM. Also, while an increase in the expressions of the p21, p27, and p53 genes was observed across all compounds in A549 cells, a decrease in the expressions of the GRP78, GRP94, AKT, RIPK1, CDK1, CDK2, HSP27, HSP40, HSP60, and HSP90 genes was observed. Besides, GRP78 and Caspase-3 were considerably increased by compounds 5 and 6. While Caspase-3, CHK1, P38, P53, and TRAILR-2 pro-apoptotic protein expressions increased, BCL-2, BCL-W, IGF-II, and NFB anti-apoptotic protein expressions decreased for all compounds. The G0/G1 phase was increased by compounds 5 and 6. Although these compounds attenuated both the S and G2/M phases. Overall, the new triazines target dysregulated cell-cycle, ER stress, and apoptotic pathways, demonstrating strong therapeutic potential in lung cancer. Notably, compounds 5 and 6 exhibited cytotoxic and pathway-modulating activities, highlighting their promise as clinically relevant lead candidates. - Source: PubMed
Mesci SedaDavarcı DeryaYazgan BurakArıman Bekir SabriYıldırım TubaŞenkuytu Elif - Atherosclerosis is a vascular disease characterized by lipid deposition, chronic inflammation, and cell death. Necroptosis, a form of programmed necrosis, plays a critical role in atherosclerosis progression. This study investigates the expression of the deubiquitinating enzyme OTUD7B in atherosclerosis and its mechanism in regulating vascular injury via the RIPK1-mediated necroptosis pathway. - Source: PubMed
Publication date: 2026/06/18
Yu LinfeiWang YulongLi YihengZhang Yu - Necroptosis is a regulated form of cell death mediated by the RIPK1/RIPK3-MLKL pathway. In humans, caspase (CASP) 8 negatively regulates the necroptotic pathway by inactivating RIPK1 and RIPK3. In teleosts and other non-mammalian vertebrates, the role of caspase in necroptosis remains to be explored. By using large yellow croaker Larimichthys crocea as a representative teleost species, this work investigated caspase-mediated regulation on teleost necroptosis. - Source: PubMed
Publication date: 2026/07/02
Wang QingyueXu HangDing XinSun Li