Ripk1
- Known as:
- Ripk1
- Catalog number:
- 049925A
- Product Quantity:
- 250ul
- Category:
- -
- Supplier:
- ABM
- Gene target:
- Ripk1
Related genes to: Ripk1
- 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
anti-RIPK1 (C-Terminus)anti-RIPK1 (N-Terminus)anti-RIPK1 / RIP (aa151-180)Anti-RIPK1, Rabbit Polyclonal to RIPK1, Isotype , Host RabbitAnti-RIPK1, Rabbit Polyclonal to RIPK1, Isotype , Host RabbitAntibody to CASP2 And RIPK1 Domain Containing Adaptor With Death Domain Protein (CRADD) Organism: Homo sapiens (Human) Type: Polyclonal Source: RabbitAntibody to CASP2 And RIPK1 Domain Containing Adaptor With Death Domain Protein (CRADD) Organism: Homo sapiens (Human) Type: Polyclonal Source: RabbitBiotin-linked Antibody to CASP2 And RIPK1 Domain Containing Adaptor With Death Domain Protein (CRADD); Reactivity: Homo sapiens (Human) Clonality: Polyclonal Source: RabbitCASP2 and RIPK1 domain containing adaptor with death domain primary antibody, Host: RabbitCASP2 And RIPK1 Domain Containing Adaptor With Death Domain Protein (CRADD) Organism: Homo sapiens (Human) Source: Escherichia coliCASP2 And RIPK1 Domain Containing Adaptor With Death Domain Protein (CRADD) Organism: Homo sapiens (Human) Source: Escherichia coliCASP2 And RIPK1 Domain Containing Adaptor With Death Domain Protein (CRADD) Organism: Homo sapiens (Human) Source: Escherichia coliCell death protein RIP,Homo sapiens,Human,Receptor-interacting protein 1,Receptor-interacting serine_threonine-protein kinase 1,RIP,RIP1,RIP-1,RIPK1,Serine_threonine-protein kinase RIPCell death protein RIP,Mouse,Mus musculus,Receptor-interacting protein 1,Receptor-interacting serine_threonine-protein kinase 1,Rinp,Rip,RIP-1,Ripk1,Serine_threonine-protein kinase RIPCRADD Gene CASP2 and RIPK1 domain containing adaptor with death domain Related articles to: Ripk1
- The functional nutraceutical Spirulina (SP) was evaluated against alcohol intoxication in mice livers, concurrently striving to elucidate its protective mechanisms in cellular death pathways: necroptosis and pyroptosis. Ethanol (ET) intoxication was induced via intake of 5% ethanol in drinking water for 10 days, succeeded by a substantial dose of 50% ethanol (4 g/kg, i.p.) on day 11. SP (250 and 300 mg/kg, p.o.) were administered to the ET-intoxicated mice one hour prior to ethanol consumption for 11 days. The two submaximal doses effectively modulated the ET-instigated hepatic abnormalities. Both doses restored the disrupted hepatic function and architecture. SP mitigated serum liver biomarkers: ALT, AST and ALP, in addition to improving survival. SP substantially modified hepatic oxidative stress by inhibiting the lipid peroxidation product MDA and elevating the antioxidant levels of SOD and GSH. Meanwhile, SP counteracted the ET-induced elevated levels of hepatic TNF-α, the necroptosis-related molecular signals; RIPK1/RIPK3/MLKL and the pyroptosis biomarkers: NLRP3/caspase-1/IL-1β. However, no extra benefit was detected with the higher dose. These findings robustly imply the hepatoprotective properties of Spirulina in alcoholism at a dose correspondent to 250 mg/kg via revoking hepatic cell death chains: necroptosis and pyroptosis. Thereby, opens a new avenue for assisting cellular repair mechanisms. - Source: PubMed
Publication date: 2026/07/20
El-Tanbouly Ghada S - The receptor-interacting serine/threonine-protein kinase (RIPK) family, particularly RIPK1, RIPK2, and RIPK3, functions as a central regulatory hub at the intersection of cell death and inflammatory signaling, critically shaping the pathogenesis of inflammatory bowel disease (IBD). These kinases exhibit context-dependent dual roles in maintaining intestinal homeostasis and driving mucosal inflammation. RIPK1 operates as a molecular switch, with its scaffold activity sustaining epithelial survival via the NF-κB and MAPK pathways, whereas its kinase activity promotes apoptosis and necroptosis under pathological conditions. RIPK2 acts as an essential adaptor downstream of nucleotide-binding oligomerization domain-containing protein 1/2 (NOD1/2), mediating antimicrobial host defense while contributing to excessive inflammation upon dysregulation. RIPK3, a core executor of necroptosis, also exerts kinase-independent immunomodulatory functions that influence tissue repair and inflammatory resolution. Dysregulation of RIPK signaling disrupts epithelial barrier integrity, amplifies inflammatory cascades, and engages in crosstalk with other programmed cell death modalities, such as pyroptosis, thereby exacerbating chronic intestinal injury. Therapeutic targeting of RIPK pathways has shown promise in preclinical models; however, achieving selective modulation that suppresses pathogenic signaling while preserving physiological functions remains a critical challenge. We propose that function-selective targeting of RIPKs, rather than complete inhibition, represents an essential direction for future IBD therapy. - Source: PubMed
Publication date: 2026/07/17
Jiang LeleGou AlongKang AnjuanYan FeixingQiao YujunXu FanxiangBai Yinliang - PANoptosis is a newly identified form of programmed cell death characterized by necroptosis, pyroptosis, and apoptosis. However, the mechanism of myocardial PANoptosis in myocardial ischemia-reperfusion (MI/R) remain unclear. Allicin is a promising drug for MI/R treatment, and the targets for myocardial PANoptosis remain to be explored. - Source: PubMed
Publication date: 2026/07/17
Liang ShichaoYin JiajieGao YijieLuo FangyuanWu SongWu DanniLin ZhaoGao TongLiu MengruJiang HongWang BaofuLi Xianlun - In recent years, PANoptosis has garnered increasing attention for its potential to promote inflammation. Nevertheless, several issues, including resistance to conventional treatment and immune evasion, correlate with inflammation in the tumor microenvironment. Controlled by the assembly of NLRP12-, ZBP1-, AIM2-, and RIPK1-PANoptosome, the newly discovered programmed cell death PANoptosis simultaneously manifests the characteristics of apoptosis, necroptosis, and pyroptosis. This review summarizes the multifaceted characteristics and the molecule determining PANoptosis sensitivity within the microenvironment. It examines the immunomodulatory function of PANoptosis in the tumor microenvironment, including how immune cells mediate PANoptosis in tumor cells and how tumor cells leverage PANoptosis to evade immune response and promote immunosupression. The crucial role of PANoptosis in immune remodeling suggests promising therapeutic strategies for tumors, such as immunotherapy and combination therapy. The induction of PANoptosis may establish a positive feedback loop that promotes immune activation and has a potential to remodel the immunosuppressive TME. Future strategies is expected to provide new directions for more precise, personalized cancer treatment. - Source: PubMed
Liu FangyuZhou XuanyiLiu ZihanLuo JingTao Qingwen - Recurrent corneal erosion (RCE) is an ocular surface disease with poor epithelial-stromal adhesion and limited therapies. This study aimed to elucidate the role of necroptosis, a pro-inflammatory form of programmed cell death, in the pathogenesis of corneal erosion. - Source: PubMed
Publication date: 2026/07/16
Shen HongyiJin JiayiZhang JianqiangShao WanwenPeng JingyiYang YanZheng YongxinZhong Liuxueying