RIPK1 Antibody
- Known as:
- RIPK1 Antibody
- Catalog number:
- XW-7754
- Product Quantity:
- 0.05 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
- N,N-dimethylformamide is a widely used industrial solvent and a well-recognized occupational hepatotoxicant, which can induce multiple forms of hepatocyte death. However, whether necroptosis, a receptor-interacting protein kinase (RIPK)-dependent programmed necrotic cell death, is the predominant form in N,N-dimethylformamide-induced hepatotoxicity remains unclear. In this study, we identified necroptosis as a major mode of cell demise induced by N,N-dimethylformamide in AML12 hepatocytes (0-40mM) and cytochrome P450 2E1-overexpressing HepG2 (CYP2E1-HepG2) cells (0-400mM). N,N-dimethylformamide-induced acute liver injury in C57BL/6 mice (2.0g/kg bw for 48h) and AML12 hepatocyte damage (40mM) were both significantly suppressed by two specific necroptosis inhibitors: necrostatin-1 (targeting RIPK1) and necrosulfonamide (targeting mixed lineage kinase domain-like protein, MLKL). Furthermore, conditioned culture medium from N,N-dimethylformamide-exposed hepatocytes induced NOD-like receptor family pyrin domain-containing 3 (NLRP3) inflammasome activation in apoptosis-associated speck-like protein containing a CARD (ASC)-expressing RAW264.7 macrophages (ASC-RAW264.7), which could be blocked by necroptosis inhibitors. Collectively, these findings strongly support a model in which acute N,N-dimethylformamide exposure triggers hepatocyte necroptosis, which in turn activates the NLRP3 inflammasome in liver macrophages and exacerbates inflammatory liver injury by secreting pro-inflammatory cytokines. - Source: PubMed
Publication date: 2026/08/15
Zhang Xiu-NingChen Jing-JingWang ShuoZhang Yan-JingWang Wei-RuZeng Tao - Glaucoma, a leading cause of irreversible blindness, is characterized by the progressive loss of retinal ganglion cells (RGCs). Beyond intraocular pressure (IOP)-dependent injury, IOP-independent pathways, specifically the self-amplifying axis between oxidative stress and the necroptotic cascade, are key drivers of disease progression. Mediated by the canonical RIPK1/RIPK3/MLKL signaling, necroptosis serves as a pivotal executioner of RGC loss. Oxidative stress functions as the critical upstream trigger that amplifies this cascade, forging a vicious cycle that demands a dual-targeted intervention strategy. To counteract this pathogenic axis, we developed a hierarchically responsive hydrogel (PD@Gel) by dispersing reactive oxygen species (ROS)-responsive Plantainoside D (PD)-loaded nanoparticles (PD@NPs) within a thiolated hyaluronic acid (HA-SH) precursor. Intravitreal injection triggers rapid elation dynamic disulfide cross-linking. The HA-SH matrix functions as a "macro-scavenger" to deplete extracellular ROS, while PD@NPs fabricated from thioether-functionalized polymers act as "ROS-capturing tentacles" to eliminate intracellular ROS and release PD. Released PD selectively inhibits the necroptotic cascade. , PD@Gel preserved mitochondrial membrane potential and attenuated necroptotic signaling, alleviating this vicious cycle. , a single intravitreal injection improved RGC survival, downregulated key necroptosis markers (p-RIPK1/p-MLKL), and partially restored visual function in a murine retinal ischemia-reperfusion (I/R) injury model. Thus, this macro-to-micro platform interferes with the self-amplifying oxidative stress-necroptosis axis, representing a potential neuroprotective strategy. - Source: PubMed
Publication date: 2026/08/07
Ren HongWu YukunYang YangLi BaigeChen YuDeng LinhuaYang QianChen ZixiWu ZhenkaiZhou XuezhiJi Dan - Aquatic ecosystems are gradually being threatened by intensive agricultural practices, especially the extensive application of pesticides. Although pesticides such as organophosphates, carbamates, pyrethroids, phenylpyrazoles, and neonicotinoids are extensively used in agriculture for pest control, their entry into aquatic environments through runoff, leaching, and atmospheric deposition poses significant risks to nontarget organisms, including fish. This study provides a comprehensive understanding of pesticide-induced toxicity in fish, with particular emphasis on histopathological modifications and genetic alterations in the liver as critical biomarkers of cellular dysfunction, tissue injury, and toxicological responses. At the molecular level, the principal pathways affected included apoptosis (bcl2, caspase 3, 8, and 9), necroptosis (mlkl, ripk1, and ripk3), autophagy (atg and lc3), inflammation (cyp19a, nfκb, tnfα, and nox4), and DNA damage response pathways (atm, atr, tp53, and mdm2) indicating severe cellular stress, genomic instability, and tissue dysfunction induced by pesticide exposure. The major histopathological alterations observed in the liver included vacuolization, hemorrhage, vascular congestion, pyknotic nuclei, and inflammatory cell infiltration. This review highlights an integrated understanding of the association between hepatic histopathological manifestations and molecular responses in fish exposed to pesticides, providing insights into the mechanisms of hepatotoxicity and recognizing possible biomarkers for environmental monitoring and ecotoxicological risk assessment. These biomarkers play a crucial role in assessing the extent of aquatic contamination and understanding the implications of pesticide exposure on fish health, biodiversity, and ecosystem stability. Furthermore, this review underscores the urgent need for effective monitoring and mitigation strategies to safeguard aquatic life and maintain environmental integrity. - Source: PubMed
Publication date: 2026/08/13
Kumar ManojYadav SeemaDubey AasthaJain AnamikaSingh Shefalee - Acute liver failure (ALF) is a critical syndrome characterized by massive hepatocyte death, yet the role of macrophage extracellular traps (METs) in its pathogenesis remains poorly defined. This study investigated the effect and mechanism of the immunometabolite itaconate on MET formation and hepatocyte necroptosis in LPS/D-GaIN-induced ALF. We found that MET release was significantly elevated in ALF mice and in LPS-stimulated macrophages. Scavenging reactive oxygen species (ROS) inhibited PAD4-mediated MET extrusion. Furthermore, METs promoted hepatocyte necroptosis by activating the RIPK1/RIPK3/MLKL pathway. Genetic deletion of Irg1 (encoding the itaconate-synthesizing enzyme ACOD1) exacerbated MET formation, inflammation, and liver injury, whereas 4-OI treatment conferred significant protection. Our findings reveal a novel pathogenic axis in ALF wherein itaconate inhibits ROS-PAD4-driven MET release to attenuate hepatocyte necroptosis, highlighting a potential therapeutic strategy for acute liver injury. - Source: PubMed
Publication date: 2026/08/13
Zhou PeiXiao GaochunLi JunYin KaiBao RuiZheng QiangwenTan HuayongHui YuanjianDi Ziyang - Inflammatory bowel disease (IBD) remains a major cause of morbidity, with many patients failing to achieve sustained remission and mucosal healing. Receptor-interacting protein kinase 1 (RIPK1) is a potential therapeutic target that links tumor necrosis factor receptor signaling to inflammation, apoptosis, and necroptosis, processes relevant to epithelial injury and barrier dysfunction in IBD. - Source: PubMed
Publication date: 2026/08/13
Honap SailishDignass AxelJairath VipulMagro FernandoDanese SilvioPeyrin-Biroulet Laurent