Galectin‐3 facilitates inflammation and apoptosis in chondrocytes through upregulation of the TLR ‐4‐mediated oxidative stress pathway in TC28a2 human chondrocyte cells

2021 ◽  
Author(s):  
Wan‐Ching Chou ◽  
Kun‐Ling Tsai ◽  
Pei‐Ling Hsieh ◽  
Chin‐Hsien Wu ◽  
I‐Ming Jou ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Human Chondrocyte ◽  
Oxidative Stress Pathway ◽  
Galectin 3 ◽  
Stress Pathway

Oxidative stress pathway genes and chronic renal insufficiency in Asian Indians with Type 2 diabetes

2009 ◽  
Vol 23 (2) ◽  
pp. 102-111 ◽  
Author(s):  
Arun K. Tiwari ◽  
Pushplata Prasad ◽  
Thelma B.K. ◽  
K.M. Prasanna Kumar ◽  
A.C. Ammini ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Type 2 Diabetes ◽  
Renal Insufficiency ◽  
Chronic Renal Insufficiency ◽  
Asian Indians ◽  
Oxidative Stress Pathway ◽  
Stress Pathway

The Oxidative Stress Pathway May be an Important Pathway Leading to The Recurrence of Ewing Sarcoma —— Based On Weighted Gene Co-Expression Network Analysis

2020 ◽  
Author(s):  
Jianfeng Li ◽  
Shaoyu Hu ◽  
Song Hao ◽  
Shengjia Huang ◽  
Yi Qin ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Network Analysis ◽  
Ewing Sarcoma ◽  
Underlying Mechanism ◽  
Data Sets ◽  
Oxidative Stress Pathway ◽  
Important Pathway ◽  
First Time ◽  
Stress Pathway

Abstract Background The role of gene and pathway in recurrence of Ewing sarcoma (ES) was not clear. Thus, we investigated the biological role and underlying mechanism of gene and pathway in recurrence of ES. Methods Data sets of patients with ES were collected from the GEO database. We used dataset GSE63155 and GSE63156 to construct co-expression networks by weighted gene co-expression network analysis (WGCNA). Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analyses were performed by Database for Annotation, Visualization and Integrated Discovery (DAVID). Results We can find that genes with significant interactions in the genes of the recurrence group include SRSF11, TRIM39, SOCS3,NUPL2,COPS5. They work primarily through the oxidative stress pathway. Conclusion Through our research, for the first time found that ES by SRSF11 TRIM39, SOCS3, NUPL2, COPS5 interaction, activation of phosphorylation of bone and oxidative stress is affecting tumor recurrence.

scholarly journals ALS-FTLD-linked mutations of SQSTM1/p62 disrupt selective autophagy and NFE2L2/NRF2 anti-oxidative stress pathway

Autophagy ◽  
2019 ◽  
Vol 16 (5) ◽  
pp. 917-931 ◽  
Author(s):  
Zhiqiang Deng ◽  
Junghyun Lim ◽  
Qian Wang ◽  
Kerry Purtell ◽  
Shuai Wu ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Selective Autophagy ◽  
Oxidative Stress Pathway ◽  
Stress Pathway

Polymorphisms in oxidative stress pathway genes and prostate cancer risk

2019 ◽  
Vol 30 (12) ◽  
pp. 1365-1375
Author(s):  
Zhenzhen Zhang ◽  
Duo Jiang ◽  
Chi Wang ◽  
Mark Garzotto ◽  
Ryan Kopp ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Prostate Cancer ◽  
Cancer Risk ◽  
Prostate Cancer Risk ◽  
Oxidative Stress Pathway ◽  
Stress Pathway

scholarly journals Transcriptional Inhibitors Identified in a 160,000-Compound Small-Molecule DUX4 Viability Screen

2016 ◽  
Vol 21 (7) ◽  
pp. 680-688 ◽  
Author(s):  
Si Ho Choi ◽  
Darko Bosnakovski ◽  
Jessica M. Strasser ◽  
Erik A. Toso ◽  
Michael A. Walters ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Muscular Dystrophy ◽  
Transcriptional Activation ◽  
Target Gene ◽  
Target Genes ◽  
Facioscapulohumeral Muscular Dystrophy ◽  
Oxidative Stress Pathway ◽  
Nonspecific Effects ◽  
Stress Pathway ◽  
Mouse Myoblast

Facioscapulohumeral muscular dystrophy is a genetically dominant, currently untreatable muscular dystrophy. It is caused by mutations that enable expression of the normally silent DUX4 gene, which encodes a pathogenic transcription factor. A screen based on Tet-on DUX4-induced mouse myoblast death previously uncovered compounds from a 44,000-compound library that protect against DUX4 toxicity. Many of those compounds acted downstream of DUX4 in an oxidative stress pathway. Here, we extend this screen to an additional 160,000 compounds and, using greater stringency, identify a new set of DUX4-protective compounds. From 640 hits, we performed secondary screens, repurchased 46 of the most desirable, confirmed activity, and tested each for activity against other cell death–inducing insults. The majority of these compounds also protected against oxidative stress. Of the 100 repurchased compounds identified through both screens, only SHC40, 75, and 98 inhibited DUX4 target genes, but they also inhibited dox-mediated DUX4 expression. Using a target gene readout on the 640-compound hit set, we discovered three overlooked compounds, SHC351, 540, and 572, that inhibit DUX4 target gene upregulation without nonspecific effects on the Tet-on system. These novel inhibitors of DUX4 transcriptional activity may thus act on pathways or cofactors needed by DUX4 for transcriptional activation in these cells.

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