RIPK1 Antibody (N-term)
- Known as:
- RIPK1 Antibody (N-terminus)
- Catalog number:
- AP13893a-ev20
- Category:
- -
- Supplier:
- Abgen
- Gene target:
- RIPK1 Antibody (N-term)
Related genes to: RIPK1 Antibody (N-term)
- 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 (N-term)
Related articles to: RIPK1 Antibody (N-term)
- Myelodysplastic syndromes (MDS) are a heterogeneous group of pre-leukemic diseases marked by ineffective bone marrow (BM) hematopoiesis, peripheral cytopenia, morphologic dysplasia, and an increased risk of leukemic transformation. Increased programmed cell death (PCD) of hematopoietic stem/progenitor cells (HSPCs) and its associated inflammatory BM microenvironment have been speculated to be one of the major causes of ineffective hematopoiesis. PANoptosis is a collective term for three types of PCD: pyroptosis, apoptosis, and necroptosis. All three are mediated by a very large protein complex called a PANoptosome, composed of the key mediators of the three types of PCD. We reported that the diseased cells in MDS with genetic abnormalities, especially spliceosome mutations, show aberrant hypersensitivity to PANoptotic stimuli. Our study suggests that increased PANoptosis of BM HSPCs is one of the reasons for the ineffective hematopoiesis in MDS patients, and targeting PANoptosis may be a novel treatment strategy for MDS. Here we summarize recent advances in research into PANoptosis and discuss the potential role of PANoptosis in the pathogenesis of MDS. We discuss the potential mechanisms for targeting PANoptotic pathways to treat MDS. - Source: PubMed
Publication date: 2026/07/24
Thalla RohitLamichhane JyotiLewis CameronBreslin PeterZhang Jiwang - Breastfeeding anchors infant immunity and long-term health, but its benefits are threatened by () mastitis, an increasingly prevalent condition driven by antimicrobial resistance and therapeutic limitations. Beyond compromising maternal wellness, mastitis threatens the safety and continuity of breast milk, highlighting a critical need for innovative intervention strategies. Herein, we demonstrated that α‑ketobutyrate (α-KB), a metabolite of the transsulfuration pathway, mitigated ‑induced inflammation, oxidative stress, and blood-milk barrier (BMB) disruption both and . α‑KB enhanced macroautophagic/autophagic responses, marked by increased ATG5, BECN1 (beclin 1), and LC3-II:LC3-I conversion and reduced SQSTM1/p62, through a RIPK1-lactate-TFEB axis. Specifically, it directly bound and stabilized RIPK1, elevated lactate production, and drove TFEB nuclear translocation to activate macroautophagy/autophagy and promote intracellular bacterial clearance. Molecular docking and molecular dynamics simulations suggested stable α‑KB and RIPK1 binding via hydrophobic and hydrogen bond interactions; RIPK1 knockout abolished α‑KB-induced autophagy and lactate generation, effects rescued by lactate supplementation. This study identifies a novel immunometabolic circuit linking a metabolite to RIPK1-lactate-TFEB-mediated autophagy, offering therapeutic potential against antibiotic‑resistant mastitis and presenting a new paradigm for safeguarding breastfeeding quality and infant health. - Source: PubMed
Publication date: 2026/07/23
Fu ShaodongYang ChengsenZhao ShiyangFang YingzouLi MingLu JinyeYang BoQiu YaweiWang HuanhuanZhang JinqiuXu YuanyuanMiao Jinfeng - Cardiovascular disease is traditionally viewed through fragmented lenses-atherosclerosis, ischemia-reperfusion injury, and heart failure as distinct entities. Emerging evidence positions PANoptosis, an integrated cell-death program combining pyroptosis, apoptosis, and necroptosis, as a unifying driver of inflammation and tissue destruction along the athero-myocardial axis. This synthesis reframes cardiovascular pathology as a continuum governed by shared immunometabolic triggers and coordinated cell-death machinery. - Source: PubMed
Publication date: 2026/07/23
Zhang XinLiu MengdanYang YunyunGuo Gongliang - Necroptosis is a regulated, pro-inflammatory form of programmed cell death implicated in degenerative and inflammatory diseases, with RIPK1 acting as a key upstream regulator. However, the utility of existing RIPK1 PET radiotracers, as well as various RIPK1 inhibitors, remains uncertain, as it is unclear whether they reflect total protein abundance or phosphorylation-dependent activation (pRIPK1), limiting accurate assessment of signaling. Unlike previously reported RIPK1 PET tracers that primarily reflect total RIPK1 distribution, we investigated whether [F]RIPA56-3-F ([F]) uptake is associated with RIPK1 activation-related signaling . [F] was synthesized via copper-mediated radiofluorination, and its radiochemical properties were characterized. uptake studies were performed in ARPE-19 cells under sodium iodate-induced stress to assess the relationship between [F] uptake, pRIPK1 activation, and total RIPK1 expression. dynamic PET/CT imaging was conducted to evaluate pharmacokinetics and biodistribution. A retinal injury model induced by sodium iodate was used for time-course imaging and quantitative analysis of radiotracer uptake. Pharmacologic validation was performed using the RIPK1 inhibitor necrostatin-1s. Ex vivo analyses, including immunohistochemistry, were conducted to correlate PET findings with pRIPK1 expression. [F] was obtained with a non-decay-corrected radiochemical yield of 37.7 ± 6.1% (n = 27), radiochemical purity >99%, and stability up to 4.5 h. In ARPE-19 cells, [F] uptake increased in parallel with early pRIPK1 activation and decreased at later time points despite sustained total RIPK1 expression. dynamic PET demonstrated favorable pharmacokinetics, with a pseudo-steady state observed at 60-80 min postinjection. Time-course analysis revealed that tracer uptake peaked at early stages (7-12 h) following sodium iodate administration and declined thereafter, consistent with transient pRIPK1 activation. In the retinal injury model, ocular uptake of [F] was significantly higher than in controls (3.38 ± 0.45 vs 1.52 ± 0.21%ID/g; < 0.0001) and was significantly reduced by necrostatin-1s treatment ( = 0.0096). PET signal was detectable prior to overt structural degeneration and correlated with increased pRIPK1 expression. [F] uptake was more closely associated with pRIPK1-related signaling activity than with total RIPK1 expression, enabling noninvasive imaging of necroptosis-associated signaling . This activation-state imaging approach allows detection of early molecular events preceding structural damage and supports the use of [F] as a potential pharmacodynamic biomarker for assessing RIPK1 pathway engagement and therapeutic modulation. - Source: PubMed
Publication date: 2026/07/22
Park Sun MiLee Tae SupLee JieunYoon JiwonKim Bom SahnMoon Byung Seok - Sepsis remains a leading cause of death, driven not only by early hyperinflammation but also by a catastrophic collapse of adaptive immunity during the late phase. This failure is orchestrated by distinct regulated cell death (RCD) pathways - apoptosis, pyroptosis, necroptosis and ferroptosis - that differentially deplete T cells, B cells and dendritic cells while shaping the immunological milieu. Apoptosis silently eliminates lymphocytes and promotes immunosuppression; pyroptosis and necroptosis release damage-associated molecular patterns, fueling inflammation that paradoxically destroys adaptive effectors; and ferroptosis, an iron-dependent lipid peroxidation process, selectively targets metabolically active CD8 and T helper cells. This review proposes that these pathways do not operate in isolation but converge on a "cell death decision network" centred on caspase-8, receptor-interacting serine/threonine-protein kinase 1(RIPK1), reactive oxygen species (ROS) and mitochondria, whose integration determines lymphocyte fate under septic stress. Understanding this network opens opportunities for precision immunotherapy. Emerging strategies targeting these pathways hold promise, but their success will require phase-specific application, biomarker-guided patient stratification and cell-type-selective delivery. Targeting the quality, as well as the quantity, of cell death may restore adaptive immunity and improve survival in sepsis. - Source: PubMed
Publication date: 2026/07/22
Li XiaofangQian WeiweiCao NaHe Yarong