Results 101 to 110 of about 102,344 (304)

NLRP3 Inflammasome May Be a Biomarker for Risk Stratification in Patients with Acute Coronary Syndrome

open access: yes, 2022
De-Gang Mo,1 Lin Wang,2 Qian-Feng Han,1 Kang Yu,3 Jia-Hui Liu,1 Heng-Chen Yao1 1Department of Cardiology, Liaocheng People’s Hospital Affiliated to Shandong First Medical University, Liaocheng, People’s Republic of China; 2Cardiologic Color Doppler Room,
Mo DG   +5 more
core  

Porcine Deltacoronavirus M Protein Binds NLRP3 to Promote Inflammasome Assembly via Competition with TRIM31

open access: yesAdvanced Science, EarlyView.
Porcine deltacoronavirus (PDCoV) infection induces severe intestinal inflammation and acute diarrhea in piglets, yet the molecular mechanism remains incompletely understood. The M protein activates NLRP3 inflammasome through dual mechanisms: direct binding to the NLRP3 LRR domain and disruption of TRIM31‐mediated K48‐linked ubiquitination.
Jinhui Hou   +11 more
wiley   +1 more source

Boron-Based Inhibitors of the NLRP3 Inflammasome [PDF]

open access: yesCell Chemical Biology, 2017
NLRP3 is a receptor important for host responses to infection, yet is also known to contribute to devastating diseases such as Alzheimer's disease, diabetes, atherosclerosis, and others, making inhibitors for NLRP3 sought after. One of the inhibitors currently in use is 2-aminoethoxy diphenylborinate (2APB).
Baldwin, Alex   +19 more
openaire   +3 more sources

Targeted Degradation of STING by a Neutrophil Membrane‐Coated Nanoplatform Suppresses Microglial Pyroptosis After Subarachnoid Hemorrhage

open access: yesAdvanced Science, EarlyView.
MG1@NM‐Px serves as a microglia‐targeted STING‐degrading nanoplatform for subarachnoid hemorrhage. Following systemic administration, it crosses the blood–brain barrier and accumulates in activated microglia. STP1‐mediated STING ubiquitination and degradation suppress MAPK/inflammasome signaling, GSDME‐mediated pyroptosis, and IL‐1β release, revealing ...
Ruotian Zhang   +13 more
wiley   +1 more source

Paxillin mediates ATP-induced activation of P2X7 receptor and NLRP3 inflammasome

open access: yesBMC Biology, 2020
Background Extracellular adenosine triphosphate (ATP), a key danger-associated molecular pattern (DAMP) molecule, is released to the extracellular medium during inflammation by injured parenchymal cells, dying leukocytes, and activated platelets.
Wenbiao Wang   +18 more
doaj   +1 more source

Membrane‐Active Peptide Protects Against Inflammation by Targeting NLRP3 Activation at the Trans‐Golgi Network

open access: yesAdvanced Science, EarlyView.
The membrane‐active peptide Pep19‐2.5 reduces harmful inflammation by blocking activation of the NLRP3 inflammasome at trans‐Golgi network membranes. By targeting key membrane interactions, Pep19‐2.5 suppresses inflammatory IL‐1β production and alleviates allergic airway inflammation in mice, leading to reduced immune cell infiltration and improved ...
Jonas Engelhardt   +16 more
wiley   +1 more source

Hollow Cu2O Nanozymes Enhance Probiotic Therapy for Colitis via Redox Homeostasis and TXNIP/NLRP3 Inflammasome Inhibition

open access: yesAdvanced Science, EarlyView.
Hollow cuprous oxide (H‐Cu2O) nanozymes feature enlarged catalytic surfaces for superior reactive oxygen species (ROS) scavenging. By efficiently neutralizing mucosal ROS, H‐Cu2O directly suppresses the TXNIP/NLRP3 inflammasome axis and restores intestinal epithelial barrier integrity.
Guangzhao Wang   +7 more
wiley   +1 more source

The NLRP3-Inflammasome in Health and Disease

open access: yesInternational Journal of Molecular Sciences, 2022
The nucleotide-binding domain (NOD)-, leucine-rich repeat (LRR)-, and pyrin domain (PYD)-containing protein 3, NLRP3, is a multiprotein complex belonging to the innate immune system that can be activated by pathogens or danger-associated molecular patterns [...]
openaire   +2 more sources

QRICH1 Disrupts Endoplasmic Reticulum Homeostasis and Amplifies NF‐κB Signaling in Periodontal Ligament Stem Cells to Exacerbate Diabetic Periodontitis

open access: yesAdvanced Science, EarlyView.
QRICH1 has been established as a key factor contributing to impaired osteogenic potential and accelerated apoptosis of PDLSCs in diabetic periodontitis. QRICH1 not only significantly enhances UPR‐associated apoptotic signaling but also amplifies NF‐κB‐mediated inflammatory responses. Its inhibition restores osteogenic capacity and reduces alveolar bone
Han Li   +9 more
wiley   +1 more source

Fatty acid synthesis promotes inflammasome activation through NLRP3 palmitoylation

open access: yesCell Reports
Summary: Despite its significance, the role of lipid metabolism in NLRP3 inflammasome remains elusive. Here, we reveal a critical role for fatty acid synthase (FASN) in NLRP3 inflammasome activation.
Stuart Leishman   +5 more
doaj   +1 more source

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