Results 121 to 130 of about 134,020 (288)

SAR Studies on the Inhibitors for the Treatment of Inflammatory Diseases [PDF]

, 2016
School of Molecular Sciences(Chemistry)Inflammation is defensive host response that occurs from infection and injury and the inflammatory process is the pivotal physiological response of our body and essential part of the human physiology.
Kim, Min-Jeong
core  

Pinosylvin Inhibits Inflammatory and Osteoclastogenesis via NLRP3 Inflammasome

Advanced Science, EarlyView.
Pinosylvin blocks LPS and RANKL induced NEK7/NLRP3 interaction, inhibiting NLRP3 inflammasome oligomerization and assembly, reducing IL‐1β maturation and GSDMD cleavage, and improving the inflammatory microenvironment and abnormal osteoclastogenesis. Abstract Pro‐inflammatory cytokines such as TNF, IL‐1, and IL‐6 trigger aberrant osteoclastogenesis and
Wei Zhang, Xiangbing Wu, Wenming Li, Haifeng Zhang, Yijun Wang, Jing Xu, Wenhao Li, Yi Qin, Zebin Wu, Gaoran Ge, Shujun Lv, Lu Mao, Liangliang Wang, Dechun Geng   +13 more
wiley   +1 more source

Ubiquitination‐Dependent LLGL2 Degradation Drives Colorectal Cancer Progression via THBS3 mRNA Stabilization

Advanced Science, EarlyView.
During the progression of CRC, MDM2, as an E3 ubiquitin ligase, promotes the degradation of the LLGL2 protein. Reduced expression of the LLGL2 protein leads to the loss of support for the CNOT1 protein, decreasing the degradation of THBS3 mRNA. The increased THBS3 further activates the PI3K‐Akt pathway, promoting the proliferation and metastasis of CRC.
Jiayan Huang, Tiantian Zhang, Huimin Li, Zidan Li, Shuangshuang Yin, Yiman Liu, Chunze Zhang, Yuling Qiu, Haiyang Yu   +8 more
wiley   +1 more source

The TET3/GATA6 Axis Drives Lipid Metabolism and Therapeutic Vulnerabilities in Pancreatic Ductal Adenocarcinoma

Advanced Science, EarlyView.
The DNA demethylase TET3 drives lipid metabolic reprogramming in pancreatic ductal adenocarcinoma via a non‐catalytic mechanism. TET3 recruits histone deacetylases to repress GATA6, sustaining lipogenic enzyme expression and ferroptosis resistance.
Shuai Liu, Shaobo Kang, Na Lin, Wenqi Zhang, Shiwen Wang, Yuqing Ren, Xiaofan Ding, Jianxiu Yu, Ruiyu Xie   +8 more
wiley   +1 more source

Novel ATR/PARP1 Dual Inhibitors Demonstrate Synergistic Antitumor Efficacy in Triple‐Negative Breast Cancer Models

Advanced Science, EarlyView.
Novel ATR/PARP1 dual inhibitors are developed for the first time. Advanced lead B8 effectively reduces cell viability in vitro and suppresses tumor growth in vivo, with better potency than ATRi and PARPi alone or in combination. Mechanistically, B8 induces apoptosis, arrests the cell cycle, and inhibits cancer cells colony formation, migration, and ...
Yuan Gao, Jiawei Zhou, Chen‐Chen Wang, Zong‐Hao Wang, Nian‐Dong Mao, Meng‐Lan He, Peng‐Peng Zhang, Ping Huang, Guo‐Wei Ye, Yu‐Qing Zhang, Feng‐Hui Tang, Hang Zhang, Tian Xie, Xiang‐Yang Ye   +13 more
wiley   +1 more source

Novel Cyano‐Artemisinin Dimer ZQJ29 Targets PARP1 to Induce Ferroptosis in Pancreatic Cancer Treatment

Advanced Science, EarlyView.
A novel artemisinin derivative dimer has been synthesized, and its significant potential as an anti‐cancer agent. The study indicated that ZQJ29 effectively inhibited the proliferation of pancreatic cancer cells in vitro and in vivo. Additionally, these investigations have unveiled ZQJ29 as a new potent PARP1 inhibitor, with the capability to induce ...
Jianping Chen, Lingyun Yue, Yanna Pan, Bingying Jiang, Junfeng Wan, Haixia Lin, Fujiang Guo, Huiyu Li, Yajuan Li, Qingjie Zhao   +9 more
wiley   +1 more source

Nephronectin (NPNT) is a Crucial Determinant of Idiopathic Pulmonary Fibrosis: Modulating Cellular Senescence via the ITGA3/YAP1 Signaling Axis

Advanced Science, EarlyView.
Through a comprehensive multi‐omics analysis, this study identifies a marked reduction in Nephronectin (NPNT) expression within fibrotic lung tissue. This reduction impairs the binding capability to the ITGA3 receptor, consequently causing YAP1 to persist in the cytoplasm, where it undergoes degradation.
Jiayu Guo, Yan Wang, Qiudi Liu, Zhaoyang Luo, Xiaomu Tian, Yuquan Wang, Yang Liu, Zhiwei Ning, Yingying Guo, Huiying Gao, Xinyue Wang, Jinglong Feng, Mengmeng Liu, Dina Saifullina, Yixin Zhang, Tengfei Pan, Yu Bian, Tao Ban, Tianyu Li, Yunyan Gu, Haihai Liang   +20 more
wiley   +1 more source

The GRK2/AP‐1 Signaling Axis Mediates Vascular Endothelial Dysfunction and Atherosclerosis Induced by Oscillatory Low Shear Stress

Advanced Science, EarlyView.
This study highlights GRK2 is a central mediator in OSS‐induced endothelial dysfunction. OSS activates GPCRs in endothelial cells, leading to GRK2 phosphorylation and the activation of AP‐1. AP‐1 induces inflammation, while also promoting NR4A1 expression and anchoring LKB1 in the nucleus, which suppresses AMPK activity. This cascade causes endothelial
Li‐Da Wu, Yi Shi, Chao‐Hua Kong, Ai‐Qun Chen, Ying Kang, Jun‐Yan Kan, Xiao‐Min Jiang, Peng Chu, Dong‐Chen Wang, Yi‐Fei Lv, Zhi‐Yuan Qian, Zi‐Hao Jiang, Yun‐Wei Chen, Yue Sun, Rui‐Rui Chang, Wen‐Ying Zhou, Yue Gu, Jun‐Xia Zhang, Shao‐Liang Chen   +18 more
wiley   +1 more source

Activation of Kir4.1 Channels by 2‐D08 Promotes Myelin Repair in Multiple Sclerosis

Advanced Science, EarlyView.
Multiple sclerosis causes myelin loss and neurological dysfunction. This study shows that 2‐D08, a small molecule targeting Kir4.1 channels, promotes OPCs differentiation via FYN tyrosine kinase phosphorylation and the FYN/MYRF pathway. It significantly improves myelin repair and motor deficits in EAE mice and marmosets, highlighting its potential as a
Mingdong Liu, Shengyu Jin, Xin Fu, Chong Xie, Yi Chen, Liangtang Chang, Yongheng Fan, Donghua He, Xiaoqi Hong, Xi Shen, Xiaoli Zheng, Qiyue Wang, Dao Shi, Fangyuan Li, Daishun Ling, Yangtai Guan, Neng Gong, Xiaoping Tong   +17 more
wiley   +1 more source

Long Term High‐Salt Diet Induces Cognitive Impairments via Down‐Regulating SHANK1

Advanced Science, EarlyView.
The study identifies a novel mechanistic link between long‐term HS diet and cognitive impairment, wherein PKA/CREB axis inactivation leads to SHANK1 reduction, synaptic damage, and cognitive deficits. Abstract High‐salt (HS) diet is an established risk factor for cognitive impairment, but the underlying mechanisms remain unclear.
Cuiping Guo, Yuanyuan Li, Wensheng Li, Tongrui Wu, Yi Liu, Yacoubou Abdoul Razak Mahaman, Jianzhi Wang, Rong Liu, Wei Liu, Hui Shen, Xiaochuan Wang   +10 more
wiley   +1 more source