RIPK1 Antibody (OALA06017)
- Known as:
- RIPK1 Antibody (OALA06017)
- Catalog number:
- oala06017
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Aviva Systems Biology
- Gene target:
- RIPK1 Antibody (OALA06017)
Related genes to: RIPK1 Antibody (OALA06017)
- 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 (OALA06017)
Related articles to: RIPK1 Antibody (OALA06017)
- Immune checkpoint inhibitors (ICIs) are first-line therapy for cervical cancer (CC), yet their efficacy is limited to a subset of patients owing to low tumor immunogenicity. Single-cell RNA sequencing revealed that CC patients exhibiting robust immune responses following radiotherapy (RT) showed upregulation of necroptosis along with lower baseline RIPK1 expression. In vitro and in vivo experiments further illustrated that RT alone upregulates RIPK1 expression. Inspired by these findings, we developed a hafnium (Hf)-based nanoscale metal-organic framework loaded with LD4172, a RIPK1 degrader (LD4172/Hf). The combination of RT and LD4172/Hf effectively induced necroptosis, and elicited a potent immune response via triggering necroptosis-mediated immunogenic cell death (NICD). This effect was characterized by enhanced macrophage infiltration and phagocytosis, increased M1 polarization, reduced M2 polarization, and improved antigen presentation capacity in macrophages. Furthermore, combined RT + LD4172/Hf with PD‑1 blockade amplified the anti‑tumor immunity driven by NICD. This combined treatment nearly doubled the production of tumor-killing cytokines (IFNγ and GZMB) in CD8 T cells and promoted the expansion of CD44⁺ effector memory T cells upon tumor rechallenge, compared with RT plus PD-1 blockade alone, thereby enabling efficient tumor elimination and conferring protection against tumor relapse. Collectively, these findings position LD4172/Hf in combination with radio-immunotherapy as a promising therapeutic strategy for CC patients. - Source: PubMed
Publication date: 2026/08/22
Wu TongLv BinWang HanHe GuangpingFu YuandongJi XiuruZeng YulianNi DalongQiu JunjunHua Keqin - Inflammatory bowel disease (IBD) is a chronic condition caused by altered cytokine signaling, maladaptive immunity, dysbiosis, and intestinal barrier dysfunction. Although current therapies aim to correct these imbalances to induce remission, most patients ultimately relapse, suggesting that key pathogenic mechanisms persist. Here, we identified aberrant epithelial cell death signaling as an underlying feature of IBD that arises in patients in remission and on advanced therapy. Mechanistically, nascent inflammation skewed epithelial cells into an M1-macrophage-like transcriptional state that promoted RIPK1-independent necroptotic signaling. This signaling then triggered inducible nitric oxide synthase-assisted mitochondrial apoptosis of absorptive epithelial cells and PUMA-mediated intestinal stem cell death. Thus, aberrant epithelial cell death signaling represents a hallmark of IBD that occurs early in mucosal lesion development, persists despite current therapeutic strategies, and predicts clinical relapse. - Source: PubMed
Publication date: 2026/08/27
Pang JiyiAl-Ani Aysha HPatel Komal MZhou YunzhuoYoung Samuel NChen JinjinKong IsabellaBarrios MarilouRickard James AChen SiqiMa XiuquanShojaee FarzanehKim Seong-BeomForoughi SiavashCawthorne WayneJacobsen Annette VJois AshaWeir Ashley LWhitehead Lachlan WRajasekhar PradeepHorne Christopher RLyu RuqianMather Lucy JYip Raymond K HTsui EllenAzeez ImadhTan TaoLiang WeiweiSivanesan SureshMetz AndrewPatwardhan AshShea NatalieIyngkaran GuruSchneider DanielElford Alexander TBeattie WilliamMacrae FinlayLiccardi GianmariaWalczak HenningZhang YuxiaSieber Oliver MSpelman TimGiulino-Roth LisaChristie MichaelChen YunshunRogers Kelly LBowden RoryNicholson Sandra ELawlor Kate EHawkins Edwin DChristensen BrittSamson Andre LVince James EMurphy James M - In contrast to foreign nucleic acids, some of our own endogenously synthesized nucleic acids may become immunologically active without being considered "foreign". For example, abnormalities in chromatin organization, transcription termination, ribonucleic acid (RNA) splicing, and RNA editing, together with damage to mitochondrial integrity, may render normally functional deoxyribonucleic acid (DNA) and RNA persistently available and aberrantly structured ligands for innate immunity. Z-DNA-binding protein 1 (ZBP1), recently identified as an important component of this innate immune system, recognizes both left-handed DNA (Z-DNA) and left-handed RNA (Z-RNA) using its tandem Z-alpha (Zα) domains and couples recognition of these conformational states to receptor-interacting serine/threonine-protein kinase 1 (RIPK1)-, receptor-interacting serine/threonine-protein kinase 3 (RIPK3)-, and mixed-lineage kinase domain-like pseudokinase (MLKL)-dependent inflammatory and cell-death pathways. More recent studies have also shown that ZBP1 plays a role in recognizing damaged self-nucleic acids associated with tauopathies, Alzheimer's disease (AD), traumatic brain injury (TBI), and amyloid-associated neuroinflammation. The nucleic-acid forms associated with these conditions include transposable-element activation, extended repeat-containing transcripts, RNA-RNA duplexes or RNA:DNA hybrids, oxidized mitochondrial DNA (mtDNA), and intercellularly transferred nucleic acids, all of which may exhibit substrate structures compatible with Z-form formation. Signaling by ZBP1 does not occur simply based upon nucleic-acid abundance; rather, signaling occurs after prolonged exposure to a nucleic acid when it persists in a structurally competent state, sufficient receptors are present to bind its exposed regions, the receptor proteoforms are competent to participate in signaling, receptor-interacting protein homotypic interaction motif (RHIM)-dependent assembly occurs, and the appropriate adaptor molecules are present. Furthermore, the identity of the cell type expressing ZBP1 determines whether the response produces RIPK3-MLKL-dependent neuronal injury, microglia-mediated inflammation, apoptosis, or mixed cell death. Finally, competition with adenosine deaminase acting on RNA 1 (ADAR1), melanoma differentiation-associated protein 5 (MDA5), double-stranded RNA-dependent protein kinase (PKR), the cyclic guanosine monophosphate-adenosine monophosphate synthase-stimulator of interferon genes (cGAS-STING) pathway, and other nucleic-acid-sensing proteins divides the available pool of endogenous nucleic acids among the outcomes of immune tolerance, type I interferon (IFN-I) signaling, translational inhibition, neuroinflammation, and necroptosis. - Source: PubMed
Publication date: 2026/08/21
Șerban MateiToader CorneliuCovache-Busuioc Răzvan-Adrian - Across all domains of life, functional amyloid fibrils serve structural, storage and signalling functions. In signalling pathways, assembly into the amyloid state constitutes a rapid and cooperative molecular switch that can reorganise protein function, promote multivalent interactions, and amplify downstream responses through templated self-propagation. Advances in the understanding of functional amyloids as regulators of signalling highlight their tailored structural properties and biological consequences. The nucleation-dependent polymerisation of amyloid enables sensitive control over activation thresholds, while the repetitive fibrillar architecture concentrates functional domains to enhance avidity and cooperativity. Controlled mechanisms for assembly, compartmentalisation and reversibility prevent inappropriate persistence or activity. These features underpin diverse signalling systems, including the RIPK1:RIPK3 necrosome in mammalian necroptosis, fungal prion-based cell-death pathways and prion-like regulatory systems in yeast and metazoans that modulate translation, development and cellular memory. Functional amyloids represent a versatile and evolutionarily conserved mechanism for molecular signalling and offer opportunities for the design of programmable amyloid-based switches with potential applications in therapeutics and synthetic biology. - Source: PubMed
Buchanan Jessica AWilliams Brayden CSteain MeganSunde Margaret - Neuroinflammation is no longer a secondary feature of amyotrophic lateral sclerosis (ALS), but rather a disease-modifying process that actively shapes the motor neuron vulnerability from the earliest stages of pathology. Central and peripheral immune cells, including microglia, astrocytes, and infiltrating T lymphocytes, adopt context-dependent states that can be neuroprotective or neurotoxic depending on disease stage and genetic background. These states are driven by discrete molecular programs, such as cGAS-STING-mediated innate immune sensing, NLRP3 inflammasome activation, and RIPK1-dependent necroptotic signaling, which represent tractable therapeutic targets. The repeated failure of broad-spectrum immunosuppressive trials reflects a fundamental mismatch between the non-selective interventions and the mechanistically distinct immune states of diseases. Converging transcriptomic, genetic, and immunophenotypic evidence supports the existence of putative neuroimmune endotypes in ALS, though this framework remains a working hypothesis pending prospective validation in biomarker-stratified cohorts. Advances in the following three domains are needed for realizing precision immunotherapy: standardized biomarker panels (including cerebrospinal fluid chitinases and TSPO-PET) to stratify patients by inflammatory subtype; pharmacodynamic readouts to confirm target engagement before interpreting clinical outcomes; and adaptive platform trial designs capable of evaluating mechanism-matching interventions in defined subgroups. This review integrates ALS-associated neuroinflammation with emerging precision medicine strategies, arguing that the central translational question is no longer whether or not to target neuroinflammation, but how, when, and in whom neuroinflammation should be targeted. - Source: PubMed
Publication date: 2026/08/24
Tang LuFan Dongsheng