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
- Receptor-interacting protein kinase 1 (RIPK1) is a critical regulator of programmed cell death and is implicated in various pathological conditions, particularly in mediating tumor resistance to immune checkpoint inhibitors (ICIs). In this study, we have pioneered the development of a novel cereblon (CRBN)-recruiting RIPK1 degrader, LD5095, through systematic optimization of linker and CRBN ligand portion. LD5095 demonstrates potent and selective RIPK1 degradation across cell lines, with rapid kinetics and sustained degradation over 72h postwashout. Functionally, RIPK1 degradation by LD5095 significantly sensitized Jurkat cells to TNFα-induced apoptosis. Furthermore, LD5095 exhibited favorable pharmacokinetics, including metabolic stability and an extended half-life. Strikingly, in vivo, a single dose of LD5095 achieved durable RIPK1 degradation in xenograft tumors over 6 days. These findings underscore the potential of LD5095 as a chemical probe for studying RIPK1 biology and a promising candidate for cancer treatment. - Source: PubMed
Lu DongYu XinLin HanfengCheng RanZhang MinYang BinChen JingjingLi FengQi XiaoliWang Jin - Regulatory T (Treg) cells hold great promise as next-generation therapeutics for autoimmune diseases. However, maintaining their functional persistence within inflamed tissues remains a major translational challenge. Using an in vitro system that recapitulates the inflammatory CNS milieu of multiple sclerosis (MS), together with a pooled shRNA screen, we identify necroptotic signaling as a key driver of Treg cell death, thereby compromising Treg functional persistence under inflammatory conditions. We further demonstrate that Treg cells in both a mouse model of MS and patients with MS exhibit a preferential susceptibility to RIPK1 kinase-dependent necroptosis. Mechanistically, a FOXP3-driven low-glucose metabolic program renders Treg cells intrinsically susceptible to necroptosis by limiting O-GlcNAc modification on RIPK1. This vulnerability is not shared by conventional T cells under comparable inflammatory conditions. Finally, in combined with adoptive Treg cell transfer, we show that selective inhibition of necroptosis in Treg cells enhances their survival and suppressive function at sites of active inflammation, thereby reducing autoimmune pathology in mouse models of MS and systemic lupus erythematosus. Together, these findings identify necroptotic cell death as a barrier to Treg persistence within inflamed tissues and highlight the therapeutic potential of necroptosis-resistant Treg cells for the treatment of autoimmune diseases. - Source: PubMed
Publication date: 2026/09/01
Wu QiaoyanCui NaGao LiLu ZhihuiAo XiangPang RuiLi XingyanPan HelingXu DaichaoLi PeiyingYuan JunyingZou Chengyu - Microglia are central mediators of neuroinflammation following ischemic stroke. Our previous multi-omics data revealed significant upregulation of leukocyte immunoglobulin-like receptor subfamily B member 4 (LILRB4) in microglia after transient middle cerebral artery occlusion (tMCAO), but its functional role remains unclear. This study demonstrates that LILRB4 expression peaks at 3 days post-tMCAO and is predominantly localized to microglia. Microglia-specific Lilrb4 knockout (Lilrb4-cKO) displayed worse neurological functions, larger infarct volumes, and more significant microglial activation. Transcriptomic analysis in vitro and functional experiments further revealed that microglial LILRB4 knockdown promoted the release of proinflammatory factors and enhanced necroptosis. Mechanistically, deletion of LILRB4 mainly drives receptor-interacting protein 3 (RIPK3) and mixed lineage kinase domain-like (MLKL) expression and phosphorylation, without affecting receptor-interacting protein 1 (RIPK1). Pharmacologic inhibition of RIPK3 can relieve the brain damage caused by LILRB4 knockout after stroke. Additional analysis showed that LILRB4 negatively regulates the stimulator of interferon genes (STING)/RIPK3 axis to limit microglial necroptosis. STING suppression blocked the hyperactivation of RIPK3 induced by LILRB4 deficiency. In conclusion, LILRB4 attenuates ischemic brain injury by suppressing STING/RIPK3-mediated microglial necroptosis and neuroinflammation, emphasizing its significance as a potential neuroprotective therapy. - Source: PubMed
Hu JinglongZhang MeijuanLiu PinyiChen YantingMeng HailanXia ShengnanBao XinyuXu YunChen Yan - Atherosclerosis is driven by the interplay between lipid accumulation, chronic inflammation, and macrophage dysfunction. Although intensive lipid-lowering therapy reduces cardiovascular risk, substantial residual risk persists, highlighting the importance of impaired macrophage cholesterol handling and reverse cholesterol transport (RCT). This review summarizes the bidirectional relationships between macrophage programmed cell death and cholesterol metabolism, with a focus on apoptosis, pyroptosis, necroptosis, and ferroptosis, which have been comparatively well studied in atherosclerosis and have direct or indirect links to macrophage cholesterol handling. Apoptosis may support plaque homeostasis when apoptotic cells are efficiently cleared by efferocytosis, thereby limiting inflammation and promoting LXR-dependent cholesterol efflux. In contrast, defective efferocytosis can lead to secondary necrosis and inflammatory amplification. Pyroptosis, necroptosis, and ferroptosis may impair macrophage cholesterol homeostasis through overlapping mechanisms involving inflammatory signaling, oxidative stress, membrane disruption, reduced ABCA1/ABCG1-dependent efflux, and HDL dysfunction. Autophagy and lipophagy exert context-dependent effects: appropriate autophagic flux facilitates intracellular cholesterol mobilization, whereas excessive or dysregulated autophagy may increase ferroptotic susceptibility through ferritinophagy, iron release, and GPX4 loss. Based on these observations, we propose a macrophage death-mode bifurcation framework centered on caspase-8 activity, RIPK1 ubiquitination, mitochondrial stress, oxidative stress thresholds, and autophagic flux. These interconnected nodes may influence whether macrophages undergo apoptosis with efficient clearance or inflammatory and lytic death associated with impaired net cholesterol flux. However, the strength of evidence differs among death modalities, and many proposed links remain indirect or primarily supported by preclinical studies. This framework provides a basis for future studies integrating cell-death regulation, cholesterol transport, and plaque stability. - Source: PubMed
Publication date: 2026/08/17
Bian YananHu Xiaoyang - Cordycepin (COR) is a natural bioactive compound derived from . Relevant studies have shown that COR can alleviate kidney damage, but the underlying mechanism of its action in the treatment of acute kidney injury (AKI) remains to be further clarified. - Source: PubMed
Fan XiuzhaoHan XiutaoZhao ZhiboLi JunhuTian ShuangshuangZhang FangZhou Xiaoshuang