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#38886341   2024/06/17 To Up

NCF4 attenuates colorectal cancer progression by modulating inflammasome activation and immune surveillance.

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Longjun Li, Rudi Mao, Shenli Yuan, Qingqing Xie, Jinyu Meng, Yu Gu, Siyu Tan, Xiaoqing Xu, Chengjiang Gao, Hongbin Liu, Chunhong Ma, Si Ming Man, Xiangbo Meng, Tao Xu, Xiaopeng Qi

1119 related Products with: NCF4 attenuates colorectal cancer progression by modulating inflammasome activation and immune surveillance.



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#38882867   2024/03/29 To Up

NLRP3 Inflammasome in Autoinflammatory Diseases and Periodontitis Advance in the Management.

Inflammatory chemicals are released by the immune system in response to any perceived danger, including irritants and pathogenic organisms. The caspase activation and the response of inflammation are governed by inflammasomes, which are sensors and transmitters of the innate immune system. They have always been linked to swelling and pain. Research has mainly concentrated on the NOD-like protein transmitter 3 (NLRP3) inflammasome. Interleukin (IL)-1 and IL-18 are pro-inflammatory cytokines that are activated by the NOD-like antibody protein receptor 3 (NLRP3), which controls innate immune responses. The NLRP3 inflammasome has been associated with gum disease and other autoimmune inflammatory diseases in several studies. Scientists' discovery of IL-1's central role in the pathophysiology of numerous autoimmune disorders has increased public awareness of these conditions. The first disease to be connected with aberrant inflammasome activation was the autoinflammatory cryopyrin-associated periodic syndrome (CAPS). Targeted therapeutics against IL-1 have been delayed in development because their underlying reasons are poorly understood. The NLRP3 inflammasome has recently been related to higher production and activation in periodontitis. Multiple periodontal cell types are controlled by the NLRP3 inflammasome. To promote osteoclast genesis, the NLRP3 inflammasome either increases receptor-activator of nuclear factor kappa beta ligand (RANKL) synthesis or decreases osteoclast-promoting gene (OPG) levels. By boosting cytokines that promote inflammation in the periodontal ligament fibroblasts and triggering apoptosis in osteoblasts, the NLRP3 inflammasome regulates immune cell activity. These findings support further investigation into the NLRP3 inflammasome as a therapeutic target for the medical treatment of periodontitis. This article provides a short overview of the NLRP3 inflammatory proteins and discusses their role in the onset of autoinflammatory disorders (AIDs) and periodontitis.
Nada Hashim, Rasha Babiker, Riham Mohammed, Mohammed Mustahsen Rehman, Nallan Csk Chaitanya, Bakri Gobara

1671 related Products with: NLRP3 Inflammasome in Autoinflammatory Diseases and Periodontitis Advance in the Management.

500 tests500 tests18 kgs500 tests500 tests

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#38882680   2024/04/22 To Up

Rational design of monomeric IL37 variants guided by stability and dynamical analyses of IL37 dimers.

IL37 plays important roles in the regulation of innate immunity and its oligomeric status is critical to these roles. In its monomeric state, IL37 can effectively inhibit the inflammatory response of IL18 by binding to IL18R, a capacity lost in its dimeric form, underlining the pivotal role of the oligomeric status of IL37 in its anti-inflammatory action. Until now, two IL37 dimer structures have been deposited in PDB, reflecting a substantial difference in their dimer interfaces. Given this discrepancy, we analyzed the PDB structures of the IL37 dimer (PDB IDs: 6ncu, 5hn1) along with a AF2-multimer prediction by molecular dynamics (MD) simulations. Results showed that the 5hn1 and AF2-predicted dimers have the same interface and stably maintained their conformations throughout simulations, while the recent IL37 dimer (PDB ID: 6ncu) with a different interface did not, proposing a possible issue with the recent IL37 dimer structure (6ncu). Next, focusing on the stable dimer structures, we have identified five critical positions of V71/Y85/I86/E89/S114, three new positions compared to the literature, that would reduce dimer stability without affecting the monomer structure. Two quintuple mutants were tested by MD simulations and showed partial or complete dissociation of the dimer. Overall, the insights gained from this study reinforce the validity of the 5hn1 and AF2 multimer structures, while also advancing our understanding of the IL37 dimer interface through the generation of monomer-locked IL37 variants.
Inci Sardag, Zeynep Sevval Duvenci, Serkan Belkaya, Emel Timucin

1915 related Products with: Rational design of monomeric IL37 variants guided by stability and dynamical analyses of IL37 dimers.

5 G500 MG 125 ml 25 mg10 nmol10 mg100ug100ul50 mg2.5 mg25 mg10 nmol

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#38881305   2024/06/25 To Up

Unlocking the novel activation mechanism of human IL-18.


Yingchao Hu, Yuxian Song, Shuo Yang

1767 related Products with: Unlocking the novel activation mechanism of human IL-18.

0.1 mg1mg200 1021 mg 100ul0.1 mg0.1ml (1mg/ml)1 mL100

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#38880358   2024/06/14 To Up

P2X7 receptor deficiency attenuates cisplatin-induced kidney injury via inhibiting NLRP3 inflammasome activation.

Nephrotoxicity is a major constraint of cisplatin application in many solid tumors. Since the lack of preventive strategies, the necessity exists to identify critical molecular targets involved in cisplatin nephrotoxicity. The Purinergic ligand-gcotedion channel 7 receptor (P2X7R) is a ligand-gated ion channel that is predominantly implicated in inflammation and cell death. Our aim is to investigate the role P2X7R in cisplatin-induced acute and chronic kidney injury, as well as the underlying mechanism. In this study, we found that cisplatin can cause an increase in the expression of P2X7R in mouse kidney tissue, and P2X7R knockout can alleviate acute renal function damage caused by cisplatin, as well as the expression of kidney injury molecule 1 (KIM-1) and interleukin-18 (IL-18). Cisplatin can cause an increase in the expression of nucleotide-binding domain-like receptor protein 3 (NLRP3) inflammasome in mouse kidney tissue. Compared with wild-type mice, P2X7R -/- mice showed decreased expression of NLRP3, apoptosis-associated speck-like protein containing a caspase recruitment domain (ASC), cleaved Caspase-1, and cleaved IL-1β in kidney tissue after cisplatin administration, and the apoptosis of renal tubular epithelial cells were also decreased. In addition, we also found that NLRP3 knockout can improve cisplatin induced degeneration, detachment, and necrosis of renal tubular epithelial cells. Furthermore, P2X7R -/- mice also showed reduced renal fibrosis and better long-term renal prognosis. In conclusion, our study identified that P2X7R knockout can improve cisplatin induced acute renal injury and chronic renal fibrosis by inhibiting the activation of NLRP3 inflammasome.
Yingying Qian, Ning Zhao, Ming Wang, Zhiguo Zou, Kewei Xie

2718 related Products with: P2X7 receptor deficiency attenuates cisplatin-induced kidney injury via inhibiting NLRP3 inflammasome activation.

100ug100ug100 ug/vial96T96T50μl200ul100.00 ul100ug

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#38878806   2024/06/13 To Up

NLRP12-associated autoinflammatory disease: A novel causal mutation and bioinformatics analyses.

Nucleotide-binding leucine-rich repeat-containing receptor 12-associated autoinflammatory disease (NLRP12-AID) is a rare autosomal dominant disorder. In this study, we reported a case of this rare disease with a novel NLRP12 mutation (A218V, rs749659859). The patient displayed typical symptoms, including recurrent fever, arthralgia, and skin allergies. Elevated serum IgE, decreased apolipoprotein A1, high-density lipoprotein cholesterol, and fluctuating levels of various leukocyte subtypes, procalcitonin, IL6, creatine kinase, and 25-hydroxyvitamin D were also detected. Inflammatory lesions were observed in multiple organs using F-FDG PET/CT. By mining single-cell transcriptome data, we identified relatively high expression of NLRP12 in monocytes compared to other human peripheral blood mononuclear cells. NLRP12-positive monocytes exhibited reduced expression of IL18, CCL3, and TNFA compared to NLRP12-negative monocytes. Structural analyses suggested that the A218V mutation, along with A218T and F402L, may reduce the ATP-binding affinity of the NLRP12 protein. These findings may provide new insights into the mechanisms of NLRP12-AID, and suggest the potential ATP-based therapy for further investigation.
Zhonghua Li, Qi Zhi, Jiahuang Li, Bo Zhu

2737 related Products with: NLRP12-associated autoinflammatory disease: A novel causal mutation and bioinformatics analyses.

1000 tests100ug10 mg50ug

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#38878634   2024/06/14 To Up

Artemisinin attenuated ischemic stroke induced pyroptosis by inhibiting ROS/TXNIP/NLRP3/Caspase-1 signaling pathway.

To explore the neuroprotective mechanism of artemisinin against ischemic stroke from the perspective of NLRP3-mediated pyroptosis.
Yue Wang, Huiling Yuan, Da Shen, Shuyuan Liu, Weiao Kong, Keying Zheng, Jiehong Yang, Lijun Ge

1699 related Products with: Artemisinin attenuated ischemic stroke induced pyroptosis by inhibiting ROS/TXNIP/NLRP3/Caspase-1 signaling pathway.

1 mg1000 assays2 Pieces/Box1000 assays 100ul1000 assays1000 assays1000 assays1000 assays100ug1 mg

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#38878489   2024/06/14 To Up

Remdesivir ameliorates ulcerative colitis-propelled cell inflammation and pyroptosis in acetic acid rats by restoring SIRT6/FoxC1 pathway.

Ulcerative colitis (UC) is a primary culprit of inflammatory bowel disease that entails prompt and effective clinical intervention. Remdesivir (RDV), a broad-spectrum antiviral nucleotide, has been found to exert anti-inflammatory effects in experimental animals.
Mamdouh A Oraby, Sherif S Abdel Mageed, Ahmed Amr Raouf, Dareen A Abdelshafy, Eman F Ahmed, Rowida T Khalil, Safwat A Mangoura, Doaa S Fadaly

1403 related Products with: Remdesivir ameliorates ulcerative colitis-propelled cell inflammation and pyroptosis in acetic acid rats by restoring SIRT6/FoxC1 pathway.

100ug Lyophilized100ug Lyophilized100ug Lyophilized2 Pieces/Box100ug Lyophilized100ug100ug Lyophilized96tests100ug Lyophilized100ug100ug Lyophilized

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#38874911   2024/06/14 To Up

The Therapeutic Potential of Neutrophil Extracellular Traps and NLRP3 Inflammasomes in Pneumonia.

Mycoplasma pneumoniae (MP) is the most common pathogen of community-acquired pneumonia in children. However, the role of neutrophil extracellular traps (NETs) in the pathogenesis of MP is unclear.
Lei Yang, Cen Zhang, Yan Liu, Huijing Bao, Zhihua Wang

1735 related Products with: The Therapeutic Potential of Neutrophil Extracellular Traps and NLRP3 Inflammasomes in Pneumonia.

96 tests96 tests

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