Results 131 to 140 of about 162,922 (305)

Single‐Cell Atlas of Subchondral Bone Marrow Lesions Reveals Proteostasis Dysfunction as a Druggable Mechanism for Early Osteoarthritis

Advanced Science, EarlyView.
This study reveals that abnormal mechanical stress downregulates the expression of HSP70 and impairs proteasome function in osteoarthritic bone cells, leading to misfolded collagen I accumulation and ER stress. When intracellular proteostasis capacity is exceeded, USP19 mediates the secretion of misfolded proteins into the extracellular space ...
Hailun Xu, Ting He, Yu Qian, Jia Li, Bowei Ni, Xiaojie Xu, Huanbo Wang, Peng Wang, Guoqing Cao, Siqi Ying, Guangyu Ding, Rong Wang, Zenghui Gu, Wei Li, Zhentao Man, Houfeng Zheng, Zhaohua Zhu, Zhen Li, Qingjun Meng, Chao Zheng, Liu Yang   +20 more
wiley   +1 more source

SKN-1/Nrf, a new unfolded protein response factor? [PDF]

PLoS Genetics, 2013
Keith P Choe, Chi K Leung
doaj   +1 more source

Tetrastigma Hemsleyanum Polysaccharide Suppresses Triple‐Negative Breast Cancer by Disrupting the Hippo‐YAP/TEAD4‐PDIA4 Axis and Endoplasmic Reticulum Stress Adaptation

Advanced Science, EarlyView.
ABSTRACT Triple‐negative breast cancer (TNBC) exhibits addiction to chronic endoplasmic reticulum (ER) stress, which sustains an aggressive metastatic phenotype through activation of the unfolded protein response (UPR). Here, we identify a previously unrecognized “ER‐stress addiction” axis in which the Hippo pathway effector TEAD4 directly ...
Yini Shang, Wentao Si, Youxue Zhang, Jialin Liu, Huaixi Zhang, Yafei Li, Hongmeng Su, Wei Jiang, Zhishan Ding, Lihong Wang   +9 more
wiley   +1 more source

Inhibition of SIRT7 Overcomes Radioresistance in Pancreatic Neuroendocrine Tumors by Reactivating MEN1 Expression

Advanced Science, EarlyView.
Pancreatic neuroendocrine tumors frequently silence MEN1 through epigenetic mechanisms. Here, SIRT7 recruits DNMT1 to the MEN1 promoter, drives hypermethylation, and enhances DNA repair. Inhibiting SIRT7 restores MEN1, reduces MRN complex abundance, impairs double‐strand break repair, and sensitizes PanNET models to radiation, supporting SIRT7 as a ...
Jianyun Jiang, Yan Wang, Yi Qin, Luohai Chen, Xiaowu Xu, Guixiong Fan, Desheng Jing, Miaoyan Wei, Xianjun Yu, Junfeng Xu, Shunrong Ji, Jie Chen   +11 more
wiley   +1 more source

The unfolded protein response signaling pathways in molluscs

Invertebrate Survival Journal, 2018
Unfolded protein response (UPR) as collective signal transduction pathways is essential for surviving the endoplasmic reticulum (ER) stress in vertebrates and invertebrates.
Y Huang, J Sun, L Wang, L Song
doaj  

Evolution of the unfolded protein response

Biochimica et Biophysica Acta (BBA) - Molecular Cell Research, 2013
The unfolded protein response (UPR) is a network of signaling pathways that responds to stress in the endoplasmic reticulum (ER). The general output of the UPR is to upregulate genes involved in ER function, thus restoring and/or increasing the capacity of the ER to fold and process proteins. In parallel, many organisms have mechanisms for limiting the
openaire   +2 more sources

Multi‐Organelle Stress‐Induced Paraptosis by a ROS‐Amplifying Nanocatalyst for Enhanced Cancer Immunotherapy

Advanced Science, EarlyView.
The engineered TF‐Fe@LC nanoplatform programs paraptotic death via multipath ROS amplification that disrupts redox homeostasis, provoking mitochondrial dysfunction, autophagic blockade, and ER stress. This caspase‐independent process elicits robust immunogenic cell death, combining with αPD‐L1 to activate systemic CD8+ T‐cell immunity and suppress ...
Zhe Yu, Haozhe Ren, Hua Li, Jinghan Zhao, Miaomiao Cao, Tian Tang, Youbei Qiao, Liting Chen, Tiehong Yang, Hong Wu   +9 more
wiley   +1 more source

Proteostasis collapse is a driver of cell aging and death. [PDF]

, 2019
What molecular processes drive cell aging and death? Here, we model how proteostasis-i.e., the folding, chaperoning, and maintenance of protein function-collapses with age from slowed translation and cumulative oxidative damage.
de Graff, Adam MR, Dill, Ken A, Santra, Mantu   +2 more
core  

Glutamine Deprivation Triggers Tribbles Homolog 3 Dependent G‐Quadruplex Resolution to Maintain DNA Repair and Tumor Survival

Advanced Science, EarlyView.
Glutamine deprivation triggers transient DNA damage yet activates adaptive repair in hepatocellular carcinoma cells. We identify TRIB3 as a stress‐induced nuclear scaffold that associates with DDX5 and G‐quadruplex DNA atBRCA1 andRAD51AP1 promoters. TRIB3 loss increases G4 accumulation, suppresses HR gene transcription, elevates γ‐H2A.X, and sensitizes
Qiang Ji, Xuedan Sun, Zhangran Sun, Mengfan Li, Xinyu Cheng, Shuai Tian, Rick F. Thorne, Jinming Li, Guangzhi Liu, Mian Wu, Xiaoying Liu   +10 more
wiley   +1 more source

The unfolded protein response in virus infections.

Frontiers in Microbiology, 2014
Shiu-Wan eChan
doaj   +1 more source