Human Polyclonal RIPK3 Ab
- Known as:
- Human Polyclonal RIPK3 Antibody
- Catalog number:
- a0665
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- ABclonal
- Gene target:
- Human Polyclonal RIPK3
Related genes to: Human Polyclonal RIPK3 Ab
- Gene:
- RIPK3 NIH gene
- Name:
- receptor interacting serine/threonine kinase 3
- Previous symbol:
- -
- Synonyms:
- RIP3
- Chromosome:
- 14q12
- Locus Type:
- gene with protein product
- Date approved:
- 1999-12-17
- Date modifiied:
- 2015-11-17
Related products to: Human Polyclonal RIPK3 Ab
Related articles to: Human Polyclonal RIPK3 Ab
- Myocardial infarction (MI) is a leading cause of morbidity and death worldwide. Endothelial cells (ECs) contribute to post-MI remodeling through angiogenesis, inflammation, and endothelial-to-mesenchymal transition (EndMT). ADAM17, a membrane-bound protease, is upregulated in ischemic heart disease, but its role in endothelial function post-MI is unknown. We investigated whether loss of endothelial ADAM17 could improve post-MI recovery using male and female mice with inducible endothelial-specific ADAM17 knockdown (Adam17/Cdhr5-Cre; Adam17). Surprisingly, male Adam17 mice exhibited compromised post-MI survival (42% death due to LV rupture vs. 13%), and progressive decline in cardiac function compared to controls (Adam17-MI). Post-MI rupture was less drastic but detected in female Adam17-MI mice. Adam17 hearts exhibited increased neutrophil infiltration, NETosis, and cytotoxic CD8 T-cell accumulation post-MI; however, depletion of these immune cells did not improve post-MI survival. Single-nuclei RNA-seq analyses identified suppression of pro-angiogenic and EndMT markers, and emergence of an EC subpopulation enriched for necroptotic markers. Decreased vascularization was confirmed in the infarcted myocardium with reduced coronary density (CD31 staining; 3-D micro-CT) and pVEGFR2 signaling. Suppressed EndMT in Adam17 mice was linked to reduced collagen crosslinking, decreased activation of the SMAD pathway (pSMAD2/3), decreased expression of lysyl oxidase and Fibronectin in infarcted myocardium. In EC-fibroblast co-cultures in vitro, endothelial Adam17 knockdown suppressed tubular formation in hypoxic conditions and reduced EndMT. Conditioned media from hypoxic EC suppressed fibroblast activation. Increased necroptosis in vivo (Adam17-MI), and in vitro (EC±hypoxia), was associated with increased TNFR1-RIPK3-RIPK1-MLKL signaling due to stabilization of TNFR1 in the absence of its ADAM17-mediated shedding. The critical role of necroptosis in impaired post-MI recovery was confirmed as inhibition of necroptosis (necrostatin-1) markedly improved post-MI survival and coronary vascularization in Adam17-MI hearts. This study demonstrates that ADAM17 regulates post-MI endothelial functions, necroptosis, vascularization, and EndMT, with necroptosis as a critical factor in post-MI adverse myocardial remodeling and survival. - Source: PubMed
Publication date: 2026/06/15
Al Rimon RazoanLi YingxiMeganathan IlamaranWang FaqiMurray Allan GOudit Gavin YEpelman SlavaClemente-Casares XavierKassiri Zamaneh - Lung ischemia-reperfusion (IR) injury is a critical clinical condition characterized by oxidative stress, inflammation, and necroptosis, often leading to severe complications. Cannabidiol (CBD), a non-psychoactive cannabinoid, has demonstrated anti-oxidant and anti-inflammatory properties, but its role in modulating lung IR injury remains incompletely understood. This study investigated the protective effects of CBD on lung IR injury in rats, focusing on the RIPK1/RIPK3 necroptosis pathway and the HIF-1α/VEGF/eNOS signaling axis. - Source: PubMed
Camas Hasan EkremSavran MehtapYildirim SerapAkin Suleyman EmreYazkan RasihIlhan IlterTepebasi Muhammet YusufSevuk Mehmet AbdulkadirOzmen Ozlem - As emerging global environmental contaminants, organic ultraviolet absorbers (OUVAs) are widely used in personal care formulations and exhibit environmental persistence and potential bioaccumulation. Among these compounds, 2-ethylhexyl salicylate (EHS) and homosalate (HMS) are the most frequently used salicylate-type UV filters in cosmetic formulations. Although an increasing number of studies have demonstrated their environmental hazards, little is known about the molecular mechanisms underlying their cytotoxicity in mammalian systems, a fundamental knowledge gap for both human health protection and the development of more environmentally friendly consumer goods. In this study, we used mouse embryonic fibroblasts (MEFs, 3T6) and zebrafish as models to assess the toxicological phenotypes of EHS and HMS in vitro and in vivo, respectively. We found that both EHS and HMS induced cellular damage characterized by oxidative stress, disrupted intracellular calcium homeostasis, mitochondrial impairment, and DNA damage. Importantly, molecular analyses further suggested the concurrent activation of two distinct regulated cell death programs: pyroptosis, as suggested by -mediated GSDMD cleavage, and necroptosis, as suggested by -mediated MLKL phosphorylation. The in vitro data have been partially validated at the level of gene expression and in developmental toxicity in the zebrafish model, providing some in vivo phenotypic and molecular correlates. While the upstream events were experimentally verified, the causal links among them remain to be further elucidated. Taken together, this work suggested that OUVA-induced toxicity is not limited to isolated oxidative damage, but may also involve the activation of two different cell death programs. These findings provide important molecular clues to understanding the potential health and ecological risks of widely used UV filters and offer a scientific basis for their more environmentally friendly safety evaluation and regulatory management, which are crucial for advancing more sustainable chemistry and safer consumer goods. - Source: PubMed
Publication date: 2026/05/26
He ChunluWang YanLin JialiangYu ZihaoShi YuanCheng JianhuaJiang YunyunHu Litao - Cell death is a fundamental biological process with critical roles in both normal physiology and pathological conditions, especially programmed cell death, such as apoptosis, necroptosis and pyroptosis. Programmed cell death is mediated by cascade signaling transduction rely on protein-protein interaction. Necroptosis mediator RIPK1, RIPK3 and MLKL have been shown to be regulated by different types of post-translational modifications (PTMs), suggesting that additional factors must associate with them during necroptosis. Proximity labeling (PL) has been used to tag and identify proteins, RNAs, or other biomolecules in close proximity (∼10-20 nm) to a target protein of interest. Therefore, utilizing proximity labeling coupled mass spectrometry to identify weak and transient interactors of necroptosis mediators, will be helpful for the further understanding of cell death mechanisms and functions. Here, in this chapter, we provide a step-by-step protocol for using TurboID-based proximity labeling to map interactors and regulators of key necroptotic proteins (RIPK1, RIPK3, MLKL and ZBP1). - Source: PubMed
Publication date: 2026/03/03
Hua JiangChan Francis Ka-Ming - Nanoplastic (NP) pollution threatens aquatic ecosystems, but concentration‑dependent molecular effects remain unclear. Using integrative transcriptomics and metabolomics, we exposed Procambarus clarkii to 200 nm polystyrene nanoplastics (0, 0.5, 1, 2 mg/L) for 28 days. Hepatopancreas analyses revealed a progressive shift from adaptive regulation at low doses to systemic dysfunction at high doses. At low concentrations, PS-NPs induced mild immune activation and ECM remodeling (upregulation of MUC17, ITGB1, CLEC17A). Medium-dose exposure triggered extensive transcriptomic and metabolic reprogramming, including DNA replication/repair activation (H2AX, MCM, PCNA), amino acid depletion, pro-inflammatory lipid accumulation, and elevated RIPK3 expression, indicative of necroptosis. High concentrations caused severe ECM disruption, immune dysregulation, DNA damage, and cell cycle alterations. Key genes (HSP90, CYCA, H2AX) and metabolites (vaccenic acid, L-isoleucine, 1-arachidonoylglycerol) were identified as potential biomarkers of PS-NP-induced stress. Overall, our findings revealed a concentration-dependent toxicological cascade and demonstrated the potential of crayfish as sentinel organisms for evaluating freshwater NP pollution. These results provided a molecular basis for environmental risk assessment and underscore the need to monitor NPs in freshwater ecosystems. - Source: PubMed
Publication date: 2026/06/10
Pu ShengyanMingming HanTay Yi JuinQing XiaoHongmei FuYiting WangZhenchao LiJingyou ZhangAbdullah Anisah Lee BintiLiang Ji