RIPK1 antibody
- Known as:
- RIPK1 (anti-)
- Catalog number:
- orb31978
- Product Quantity:
- 5 ug(Trial size)
- Category:
- -
- Supplier:
- Biorb
- 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
- - Source: PubMed
Publication date: 2026/05/27
Wu ZhuyangWang LingxiaWu XiaoxiaLi MingZhang Haibing - Receptor-interacting protein kinase-1 (RIPK1) is a serine-threonine kinase that is activated in the brain early after intracerebral hemorrhage (ICH), but its spatial and temporal course in the subacute period is unknown. We used mice deficient in RIPK1 kinase activity to investigate RIPK1 regulation of clinically relevant outcomes in a collagenase ICH model. At 35 days after ICH in wild-type males, RIPK1 was activated (increased in detergent-insoluble fractions) in striatal neurons, endothelium, and astrocytes. In neurons, RIPK1 activation was associated with loss of its regulators TAK1/TBK1, and RIPK1 regulated post-injury neuronal CaMKII𝛼 expression, pathological tau phosphorylation, and inflammasome activation. RIPK1 regulated post-injury gliosis, blood-brain barrier (BBB) damage and cognitive deficits in males. At 35 days after ICH in females, RIPK1 was activated exclusively in neurons but female neurons lacked the biochemical changes seen in males, and RIPK1 did not regulate increased gliosis, BBB damage, or most cognitive deficits in injured females. The studies are the first to describe cell-specific RIPK1 activation in the subacute period of experimental ICH and highlight important sex differences that should inform clinical trials of RIPK1 inhibitors in patients with ICH. Sex differences should be evaluated for RIPK1 in other brain injury models and neurodegenerative disease paradigms. - Source: PubMed
Publication date: 2026/10/02
Yang HongmeiDillon Brianne EliseMarzialo Dalila MaryDillon Jaina ThereseCao TianLevy Emily SPopeo LindsayJamali ShirinWootton DavidGrzegorczyk EvaBeckey Cameron MarieDavis AmirKarthik NanditaIngrando PaigeStogsdill Riley LNguyen Binh Minh NgocSirbulescu Ruxandra FDegterev AlexeiWhalen Michael JWu Limin - Innate immune signalling is uniquely driven through the formation of supramolecular organising centres (SMOCs), which couple receptor activation with downstream effector recruitment. The adaptor protein TRIF coordinates interferon, inflammatory, and cell death responses downstream of TLR3 and TLR4 activation, yet exactly how this protein drives such diverse outputs remains unresolved. Recent structural studies of recombinant TRIF, alongside single-molecule fluorescence imaging of endogenously expressed TRIF in live cells, reveal that TRIF assembles into complexes with heterogeneous size and morphology, with monomeric and low-order complexes associated with early-phase interferon signalling and mature, RIPK1-containing complexes associated with NF-κB activation. This review explores how differences in the structural architecture of the TRIFosome, from TIR-mediated oligomerisation through to RHIM-mediated cross-linking, may underlie this divergence in signalling outcome. Finally, this review discusses the translational opportunities that coordinating scaffold assembly with downstream function presents, including structure-selective therapeutics capable of shifting the balance between TRIF's signalling outputs and novel diagnostics that could be built on TRIFosome heterogeneity as a molecular fingerprint of disease. - Source: PubMed
Suresh PrasannaZhang Yu PBryant ClareKlenerman David - Ischemic stroke remains a leading cause of disability and mortality worldwide. Current neuroprotective treatments predominantly target neurons and fail to address the complex post-ischemic cell death cascades in astrocytes, the most abundant glial cells in the central nervous system, whose multimodal Programmed Cell Death (PCD) directly determines blood-brain barrier integrity, neuroinflammation, and secondary brain injury. - Source: PubMed
Publication date: 2026/09/29
Zhang LiRuan Yonglan - To systematically characterize the expression profiles of biomarkers associated with multiple programmed cell death (PCD) pathways-including apoptosis, pyroptosis, necroptosis, and ferroptosis-in pediatric intensive care unit (PICU) patients with sepsis, elucidate their associations with organ dysfunction severity and clinical prognosis, and identify independent predictors of 28-day all-cause mortality in children. - Source: PubMed
Publication date: 2026/09/15
Fu BingfengSun YingchaoZhang Xifeng