Mouse polyclonal to CIAS1 _ NALP3, Host Mouse
- Known as:
- Mouse pab CIAS1 _ NALP3, Host Mouse
- Catalog number:
- YF-PA26812
- Product Quantity:
- 50 uL
- Category:
- -
- Supplier:
- Abfron
- Gene target:
- Mouse polyclonal CIAS1 _ NALP3 Host
Related genes to: Mouse polyclonal to CIAS1 _ NALP3, Host Mouse
- Gene:
- NLRP3 NIH gene
- Name:
- NLR family pyrin domain containing 3
- Previous symbol:
- C1orf7, CIAS1, DFNA34
- Synonyms:
- AGTAVPRL, AII, AVP, FCAS, FCU, NALP3, PYPAF1, MWS, CLR1.1
- Chromosome:
- 1q44
- Locus Type:
- gene with protein product
- Date approved:
- 2001-08-28
- Date modifiied:
- 2019-04-23
Related products to: Mouse polyclonal to CIAS1 _ NALP3, Host Mouse
Related articles to: Mouse polyclonal to CIAS1 _ NALP3, Host Mouse
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Publication date: 2026/09/17
Saberi KianoushGhadiminia NikkiMamataliyev AbdumalikTuraev TelmonUmarkulova GulbahorNadjmitdinov OtabekArtikov AbdukakhkhorEshkaraev SadridinTakhirov YuldashAmirullayeva BarnoAyubova NargizaKuchkorova RanoErdanova Zamira - Ulcerative colitis (UC) is a prevalent inflammatory bowel disease that affects millions of people worldwide, for which no definitive cure currently exists. Herein, we report the discovery of a novel sesterterpenoid derivative, ColD14, with a complicated cage-like structure and contiguous stereogenic centers, which exhibits significant anti-NLRP3 inflammasome activity. Proteomic and biochemical studies identified glutamyl-prolyl tRNA synthetase (EPRS) as a direct target of ColD14. Both EPRS knockdown and pharmacological inhibition by ColD14 reduced NLRP3 inflammasome activation, underscoring the crucial role of EPRS in inflammatory processes. Mechanistically, through the molecular interaction with amino acid residues R1152, E1154, and R1278 at the ATP site, ColD14 inhibited prolyl-tRNA synthetase (ProRS) activity. This suppression triggered the amino acid response (AAR) pathway and consequently attenuated NLRP3 inflammasome activation via mitophagy regulation. In vivo, ColD14 activated the AAR signaling pathway, triggered mitophagy, and inhibited NLRP3 inflammasome activation, thereby alleviating DSS-induced colitis in mice. Taken together, our findings underscored the significance of EPRS in NLRP3 inflammasome activation and suggested that the EPRS inhibitor, ColD14, may be valuable in ulcerative colitis therapy via the EPRS-AAR-mitophagy axis. - Source: PubMed
Publication date: 2026/09/15
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Publication date: 2026/09/12
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Publication date: 2026/09/01
Jiang YuxinShi XiaoyuYang QianPang JianxinZhan PengXu ShujingWu Ting - Postoperative cognitive dysfunction (POCD) remains a clinically important problem after surgery, particularly in older and neurologically vulnerable patients. Its interpretation is complicated by heterogeneous cognitive definitions and follow-up periods, while the underlying biology appears to involve interacting inflammatory, metabolic, glial, and synaptic disturbances rather than a single pathogenic cascade. Esketamine has therefore attracted interest as a potential perioperative neuroprotective agent, but the strength of evidence differs markedly across the mechanisms proposed to explain its effects. We conducted a structured narrative review with evidence mapping of clinical and experimental studies identified in PubMed/MEDLINE and the Web of Science Core Collection, using a literature cutoff of 1 May 2026. Direct perioperative clinical and preclinical studies were distinguished from non-perioperative esketamine research, ketamine/enantiomer studies, and contextual POCD/PND biology, with greater mechanistic weight assigned to experiments incorporating pathway perturbation or rescue. The direct preclinical literature favors a multi-branch model of esketamine action. Functional evidence supports contributions from TLR4/MyD88-p38 signaling, STING/TBK1-associated inflammatory cell death, and PARP1-related autophagic regulation, while changes in NF-κB signaling, microglial BDNF-TrkB activity, and ROCK2/ADD1-associated synaptic remodeling are supported mainly by convergent molecular and functional findings. NLRP3 remains relevant to postoperative neuroinflammation but has not been established as a required upstream mediator of esketamine action, and proposed effects on the blood-brain barrier, antioxidant pathways, cholinergic signaling, and neurogenesis remain less directly supported in perioperative cognitive models. Clinical findings are less uniform. Some randomized trials suggest reductions in postoperative delirium or early postoperative cognitive decline in selected populations, whereas other adequately designed studies are neutral, and evidence for sustained cognitive protection is limited. Peripheral inflammatory, neuronal-injury, and neurotrophic biomarkers indicate biological activity but do not establish central target engagement or cognitive mediation. Taken together, the current literature supports a biologically plausible, multi-target model for esketamine, but not an established preventive effect against perioperative neurocognitive disorders. - Source: PubMed
Publication date: 2026/09/02
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