RIPK1 Antibody
- Known as:
- RIPK1 Antibody
- Catalog number:
- 5389
- Product Quantity:
- 0.5 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
- 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 - Duplication of 6p is a rare genetic syndrome of which about 25% have one or more congenital cardiac defects including cardiac septal defects, pulmonary artery hypoplasia and patent ductus arteriosus. We present the first case of a fetus with functional single ventricle and persistent truncus arteriosus during prenatal diagnosis whose genomic analysis revealed a novel pure duplication of 6p25.2-p22.3. The duplication fragment was confirmed to be associated with intrachromosomal insertion from mother via chromosome karyotype. The presentation of this case aims to expand the existing knowledge regarding this rare condition and facilitate its diagnosis in the future. Based on the comparison of cases with 6p duplication syndrome, we notice that the 6p terminal region, especially at 6p25.1 to 6p25.2, could be the critical region associated with heart complications or anomalies of the pulmonary arteries. The duplication of the potential modifier genes, RIPK1 and FARS2, were proposed to be attributed to heart defects in our study and should be further researched. - Source: PubMed
Publication date: 2026/06/18
Tang HuameiXu XiaoqingWu WeiWang YuxueHe YuyingQiu JunyingOu Tong - Progressive cardiomyocyte loss constitutes the pathological hallmark of dilated cardiomyopathy (DCM), a process driven by an intricate network of programmed cell death (PCD) pathways. This review systematically examines the molecular underpinnings and reciprocal crosstalk among six principal PCD modalities implicated in DCM: apoptosis, necroptosis, pyroptosis, autophagy, ferroptosis, and cuproptosis. Apoptosis is triggered by genetic defects-most notably titin ( truncating variants-epigenetic dysregulation, and endoplasmic reticulum stress, converging on the activation of both intrinsic and extrinsic caspase cascades. Necroptosis is distinguished by the aberrant nuclear accumulation of phosphorylated MLKL, particularly at the pThr residue, which selectively exacerbates cardiac dysfunction; upstream events governing this pathway include desmoplakin deficiency, PGC-1α downregulation, and TAB2 loss. Pyroptosis, orchestrated by the NLRP3-GSDMD-IL-1β axis, is robustly activated in the failing myocardium-often exceeding the magnitude of concurrent apoptosis-and propagates a pro-inflammatory milieu through the release of potent cytokines. Autophagy exhibits a pronounced bidirectional effect in DCM: while physiological autophagic flux exerts cardioprotective actions, impaired flux or hyperactivation accelerates cell demise. Ferroptosis is driven by the collapse of the System Xc-GPX4 antioxidant axis and dysregulation of the FSP1 shunt, culminating in lethal lipid peroxidation; this process is subject to upstream regulation by the Hippo-Mst1-NFS1 cascade and mA epigenetic modifications, and it engages in a vicious cycle with downstream inflammation and fibrosis. Cuproptosis ensues from FDX1-mediated copper binding to lipoylated tricarboxylic acid cycle enzymes, precipitating the loss of iron-sulfur cluster proteins and proteotoxic stress; bioinformatic analyses further implicate its interplay with immune infiltration. These PCD pathways do not operate in isolation but rather form a tightly woven molecular crosstalk network shared signaling nodes-including RIPK1, reactive oxygen species (ROS), mitochondrial machinery, and the caspase family-and functional compensation, thereby collectively dictating cardiomyocyte fate and disease trajectory. In light of this network-centric framework, therapeutic strategies that target critical hubs such as GSDMD, GPX4, or RIPK1, or leverage pathway interdependencies for combinatorial intervention, hold considerable promise for disrupting maladaptive feed-forward loops and preserving myocardial integrity. Future investigations should prioritize the delineation of patient-specific PCD network topologies in DCM to pave the way for precision-based therapeutic targeting. - Source: PubMed
Publication date: 2026/06/02
Qiu YueqingChen Zhenyi