RIPK1 Antibody
- Known as:
- RIPK1 Antibody
- Catalog number:
- 5389
- Product Quantity:
- 0.5 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
- 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 - Diabetic encephalopathy (DE) is a serious complication of diabetes mellitus characterized by progressive cognitive dysfunction, but its underlying mechanisms remain incompletely understood. Tau hyperphosphorylation and necroptosis are key pathological events in neurodegenerative diseases, but their roles in DE and the capacity of hydrogen sulfide (HS) to regulate these processes have not been investigated. We tested whether HS attenuates Tau hyperphosphorylation and necroptosis through the PI3K/AKT/GSK-3β signaling pathway to improve cognitive impairment in DE. In vitro, HT22 hippocampal neurons were exposed to high glucose (85 mM), and in vivo, a streptozotocin-induced diabetic mouse model was established. NaHS served as an exogenous HS donor, and LY294002 was employed as a PI3K-specific inhibitor. Phosphoproteomic analysis revealed that high glucose suppressed PI3K/AKT/GSK-3β signaling and concurrently elevated Tau phosphorylation (p-Tau) and necroptosis markers (p-RIPK1, p-MLKL). NaHS treatment activated PI3K/AKT/GSK-3β signaling, reduced p-Tau, p-RIPK1, and p-MLKL levels, and normalized necroptotic morphology observed by transmission electron microscopy. Flow cytometry and lactate dehydrogenase release assays confirmed that NaHS attenuated high glucose-induced cell death. In diabetic mice, NaHS improved spatial learning and memory in the Morris water maze and novel object recognition tests, restored hippocampal CA1 neuron survival, and upregulated synaptic proteins (PSD95, SYP). Co-immunofluorescence demonstrated colocalization of p-Tau and p-MLKL in the hippocampal CA1 region, which was reduced by NaHS. All protective effects of NaHS were partially reversed by LY294002, establishing a PI3K-dependent mechanism. Network pharmacology identified 76 HS-DE overlapping targets; machine learning ranked AKT family genes as top predictors. These findings demonstrate that HS improves DE by activating PI3K/AKT/GSK-3β signaling, attenuating Tau hyperphosphorylation and necroptosis. - Source: PubMed
Publication date: 2026/08/19
Zhang ShuhanYu ShihuiYang DanLiu YiDu Wenlong - Neurodegenerative diseases (NDs) are marked by selective neuronal vulnerability and progressive failure of neural circuits. Increasing evidence indicates that neuronal loss is not driven by a single terminal event, but emerges from interacting regulated cell death (RCD) programs. These programs are closely coupled to mitochondrial injury, proteostatic collapse, lysosomal stress, metabolic imbalance, glial state transitions, and chronic neuroinflammation. Yet, how distinct death pathways are organized across cell types, disease stages, and disease-specific microenvironments remains unresolved. This review examines RCD as an integrated pathogenic network in major NDs. Caspase and B-cell lymphoma 2 (BCL2) family signaling, receptor-interacting protein kinase 1 (RIPK1), RIPK3, and mixed lineage kinase domain-like protein activation, NOD-like receptor family pyrin domain containing 3 and gasdermin signaling, GPX4-linked lipid peroxidation control, and autophagy lysosomal failure are discussed as convergent stress response modules rather than isolated pathways. Across Alzheimer's disease, Parkinson's disease, amyotrophic lateral sclerosis, and Huntington's disease, these modules shape neuronal fate through disease-specific interactions with mitochondrial dysfunction, iron dyshomeostasis, inflammasome activation, and microglial metabolic remodeling. We further evaluate emerging therapeutic strategies that target cell death crosstalk, restore autophagy lysosomal competence, or improve delivery to the central nervous system, highlighting the importance of molecular selectivity, cellular context, disease stage, and translational feasibility. - Source: PubMed
Publication date: 2026/08/17
Li TianjiaoZhang QianWu YichenHuang Ruixue - Hashimoto's Thyroiditis (HT) is the leading cause of primary hypothyroidism, characterized by progressive thyroid follicular cell (TFC) loss and diffuse lymphocytic infiltration. While apoptosis dominates TFC death in HT, the role of pro-inflammatory necroptosis in TFC destruction, especially its cellular heterogeneity, spatial distribution, and inflammatory microenvironmental regulation, remains incompletely elucidated. - Source: PubMed
Publication date: 2026/08/03
Yang DongyuLu CihangTeng WeipingZhao LeiWang XichangSun YingZhang HaonanFan ShutingShi Xiaoguang