RIPK1 Antibody (OALA04372)
- Known as:
- RIPK1 Antibody (OALA04372)
- Catalog number:
- oala04372
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Aviva Systems Biology
- Gene target:
- RIPK1 Antibody (OALA04372)
Related genes to: RIPK1 Antibody (OALA04372)
- 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 (OALA04372)
Related articles to: RIPK1 Antibody (OALA04372)
- 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 - Acute myeloid leukemia (AML) remains a highly lethal hematologic malignancy, with relapse and therapeutic resistance largely driven by apoptosis evasion. Necroptosis, a regulated form of non-apoptotic cell death, has emerged as a potential strategy to eliminate apoptosis-resistant cancer cells; however, its upstream regulatory mechanisms in AML remain incompletely understood. Here, we identify the long non-coding RNA XIST as a previously underappreciated regulator of necroptosis-associated signaling in AML. XIST and CYLD were consistently downregulated in AML cell lines and primary patient samples, whereas miR-92a-3p was upregulated and inversely correlated with XIST and CYLD expression. Clinically, elevated miR-92a-3p expression was associated with inferior overall survival in AML patients. Functionally, endogenous activation of XIST significantly suppressed AML cell proliferation and induced G2/M cell cycle arrest without markedly increasing apoptosis. Instead, XIST overexpression increased membrane-disrupted cell death, as shown by trypan blue and Hoechst/PI staining, and induced necroptosis-like ultrastructural changes. XIST-mediated growth inhibition was partially rescued by the necroptosis inhibitor Necrostatin-1 but not by the pan-caspase inhibitor zVAD-fmk. Moreover, XIST overexpression enhanced CYLD expression and activated necroptosis-associated RIPK1/RIPK3/MLKL signaling, including increased phosphorylation of RIPK1, RIPK3, and MLKL. Mechanistically, XIST directly interacted with miR-92a-3p and negatively regulated its expression, while miR-92a-3p directly targeted CYLD. Inhibition of miR-92a-3p increased CYLD expression and recapitulated the anti-proliferative and necroptosis-associated effects of XIST. In vivo, XIST overexpression suppressed subcutaneous AML xenograft growth and enhanced necroptosis-associated signaling. Collectively, our findings suggest that XIST restrains AML progression, at least in part, by modulating the miR-92a-3p/CYLD axis and promoting necroptosis-associated cell death, highlighting a potential regulatory mechanism for overcoming apoptosis resistance in AML. - Source: PubMed
Publication date: 2026/07/16
Huang XianboChen YingRen YanlingWang ShashaMei ChenXu YuJin JieTong HongyanQian Jiejing