RIPK1 Antibody (OALA06017)
- Known as:
- RIPK1 Antibody (OALA06017)
- Catalog number:
- oala06017
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Aviva Systems Biology
- Gene target:
- RIPK1 Antibody (OALA06017)
Related genes to: RIPK1 Antibody (OALA06017)
- 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 (OALA06017)
Related articles to: RIPK1 Antibody (OALA06017)
- Mycobacterium tuberculosis (M. tuberculosis) has evolved to survive within host phagocytes while provoking inflammatory tissue destruction, a delicate balance that is critically shaped by programmed cell death (PCD). Rather than acting as isolated linear pathways, apoptosis, necroptosis, pyroptosis, ferroptosis, autophagy/xenophagy, ETosis/NETosis, PARP1-AIF/parthanatos-related signaling, and PANoptosis-related signaling form an interconnected network that determines macrophage fate, granuloma integrity, bacterial dissemination, and immunopathology. In this Review, we discuss how M. tuberculosis and host-derived signals engage canonical cell-death modules, including caspases, RIPK1/RIPK3-MLKL, inflammasomes-gasdermins, ROS-iron-lipid peroxidation circuits, PARP1-AIF signaling, and autophagy machinery. We highlight context-dependent effects whereby apoptosis and autophagy may promote bacterial containment, whereas necrotic and inflammatory forms of death can either enhance antimicrobial immunity or drive caseation and tissue damage. We further evaluate emerging evidence for crosstalk among PCD modalities, with particular attention to shared molecular checkpoints and the still-evolving concept of PANoptosis in tuberculosis. Finally, we discuss host-directed therapeutic strategies aimed at recalibrating, rather than simply blocking or activating, cell-death pathways. A network-based understanding of PCD in M. tuberculosis infection provides a crucial framework for developing adjunctive therapies that enhance pathogen control while limiting destructive inflammation. Unlike pathway-centered summaries, this Review reframes M. tuberculosis-induced cell death as a dynamic network in which shared molecular hubs, compensatory switching, and lesion-stage-specific microenvironments jointly determine disease outcome. - Source: PubMed
Publication date: 2026/09/07
Zhang QingChang De - β-Caryophyllene (BCP), a selective agonist of cannabinoid receptor type 2 (CB2), has garnered attention as a promising nutraceutical agent for modulating organ damage. The current study aimed at evaluating the pharmacological role of BCP in Thioacetamide (TAA)-induced liver fibrosis, with particular attention to the involvement of CB2-mediated signaling. Following the induction of fibrosis by TAA, rats were treated with BCP for 6 weeks. In a separate group, AM630, a selective CB2 receptor antagonist, was co-administered with BCP in order to validate CB2-dependent actions. TAA administration triggered significant hepatocellular injury. In addition, TAA activated necroptotic cellular death, shown in the upregulated RIPK1/RIPK3/p-MLKL expression. Growth factors' signaling was disrupted and liver regeneration was impaired. On the contrary, BCP treatment ameliorated oxidative stress, mitigated inflammation, and decreased hepatic stellate cells' activation. This was accompanied by reduced collagen deposition and attenuated fibrosis. BCP markedly abrogated necroptosis and decreased the stimulation of fibrogenic and angiogenic signaling. Additionally, BCP potentiated hepatocytes' survival and restored hepatic regenerative capacity. AM630 co-treatment abolished BCP's protective effects, confirming the CB2 receptors-dependent effects. Given findings highlight BCP as a potential therapeutic agent for liver fibrosis and delineate endocannabinoid system's role in modulating organ fibrosis. - Source: PubMed
Eddin Lujain BaderArunachalam SeenipandiLubbad LoayHammad Fayez TAdeghate ErnestSubramanya SandeepOjha Shreesh - Ulcerative colitis (UC) is a chronic inflammatory bowel disease characterized by intestinal barrier dysfunction and epithelial cell death. Necroptosis of intestinal epithelial cells (IECs) mediated by the RIPK1/RIPK3/MLKL pathway has emerged as a key driver of UC progression. Celastrol, a bioactive compound from Celastrus wilfordii, has shown anti-inflammatory potential, but its effect on necroptosis in UC remains unclear. - Source: PubMed
Publication date: 2026/08/21
Lu KeyiWang YuanyuanShi YifanLiu SiqiShao YannaWang ZhibinXu Erping - Alzheimer's disease is a complex neurodegenerative disorder characterized pathologically by amyloid-β deposition and pathological tau aggregation. Amyloid-β deposition typically occurs during the preclinical stage; however, amyloid burden does not exhibit a simple linear relationship with neurodegeneration or cognitive decline. In contrast, the spatial distribution of tau pathology is more closely associated with clinical progression. As the resident innate immune cells of the central nervous system, microglia participate in the recognition, uptake, and containment of amyloid-β and tau. Nevertheless, persistent exposure to damage-associated signals can lead to lysosomal dysfunction, dysregulated lipid metabolism, and mitochondrial impairment in microglia, thereby amplifying neuroinflammation, aberrant synaptic elimination, and neuronal injury. The traditional binary M1/M2 classification is inadequate to capture the continuous, overlapping, and context-dependent functional states of microglia, which vary across brain regions, genetic backgrounds, and disease stages. This review integrates recent evidence from genetic, single-cell/single-nucleus, and spatial transcriptomic studies and proposes a "cellular state-pathological network-therapeutic window" framework. We systematically discuss the roles of microglia in amyloid-β plaque seeding and compaction, NLRP3 inflammasome activation, mitochondrial DNA-cGAS-STING signaling, complement-mediated synaptic engulfment, and bidirectional microglia-tau feedback. On this basis, we critically evaluate the mechanistic rationale, stage dependence, and translational limitations of therapeutic axes involving TREM2/CD33, P2X7-NLRP3 and cGAS-STING, CSF1R/complement, and TNF-TNFR1-RIPK1. Current evidence suggests that the key to microglia-targeted therapy is not the broad activation or suppression of immune responses, but rather the biomarker-guided and disease-stage-specific modulation of pathogenic signaling while preserving homeostatic functions such as plaque containment, debris clearance, synaptic maintenance, and tissue repair. - Source: PubMed
Publication date: 2026/08/20
Xu LianjingZhang YingJiang LiXing Jin FengHu JingLan TianyeTa Guang - Diabetes mellitus and its complications are chronic inflammatory diseases driven by metabolic stress. PANoptosis is a recently defined inflammatory lytic cell death pathway that integrates key features of pyroptosis, apoptosis, and necroptosis, and is orchestrated by the PANoptosome complex. Emerging evidence indicates that PANoptosis plays a critical role in the pathogenesis of diabetic complications, prominently in diabetic kidney disease, retinopathy, neuropathy, and cardiomyopathy, with emerging indirect evidence from surrogate models suggesting its potential involvement in diabetic foot ulcers. In this review, we summarise the core molecular mechanisms of PANoptosis, with a focus on the crosstalk among the three programmed cell death pathways under diabetic conditions. We discuss how metabolic stressors such as hyperglycaemia, lipotoxicity, and endoplasmic reticulum stress activate distinct PANoptosome assemblies-including those involving Z-DNA-binding protein 1 (ZBP1), absent in melanoma 2 (AIM2), receptor-interacting protein kinase 1 (RIPK1), NOD-like receptor family pyrin domain-containing protein 12 (NLRP12), NOD-like receptor family pyrin domain-containing protein 3 (NLRP3), and NOD-like receptor family CARD domain-containing protein 5 (NLRC5)-thereby linking metabolic dysregulation to inflammatory cell death. Moreover, we highlight recent advances in targeting PANoptosis as a therapeutic strategy, emphasising interventions directed at upstream metabolic triggers, PANoptosome components, and downstream effector molecules. Finally, we identify key knowledge gaps and propose future research directions to facilitate clinical translation. A deeper understanding of PANoptosis in diabetic complications may pave the way for novel therapeutic approaches that simultaneously block multiple cell death pathways to ameliorate disease progression. - Source: PubMed
Publication date: 2026/08/19
Yan JinhongWang QiuyueChen Fenqin