Results 81 to 90 of about 32,322,339 (203)

Transient acceleration of autophagic degradation by pharmacological Nrf2 activation is important for retinal pigment epithelium cell survival

Redox Biology, 2018
Non-exudative age-related macular degeneration (AMD) is mainly caused by the accumulation of lipofuscin and drusen on the retinal pigment epithelium (RPE).
Yuichi Saito, Yoshiki Kuse, Yuki Inoue, Shinsuke Nakamura, Hideaki Hara, Masamitsu Shimazawa   +5 more
doaj   +1 more source

In Vivo Effect of Resveratrol-Loaded Solid Lipid Nanoparticles to Relieve Physical Fatigue for Sports Nutrition Supplements

Molecules, 2020
Resveratrol (RSV) is a natural flavonoid polyphenol compound extracted from the plants which shows various biological activities. However, the clinical application of RSV is limited by its poor aqueous solubility, rapid metabolism and poor ...
Lili Qin, Tianfeng Lu, Yao Qin, Yiwei He, Ningxin Cui, Ai Du, Jingyu Sun   +6 more
doaj   +1 more source

α‐Synuclein Promotes Atherosclerosis by Impairing Macrophage Autophagic Flux

Aging Cell, Volume 25, Issue 10, October 2026.
Extracellular α‐synuclein activates the FLOT1‐PI3K‐mTOR axis to block autophagosome‐lysosomal fusion and lipophagy, thereby promoting macrophage foaming and atherosclerosis. Knockdown of FLOT1 or inhibition of PI3K‐mTOR rescues these effects. The graphical abstract image was created with Figdraw.
Mengting Qin, Xuying Xiang, Xiaoqing Guo, Shengnan Wang, Jiaojiao Chen, Dailiang Jiang, Yuhang Feng, Jiangnan Yu, Ling Mao   +8 more
wiley   +1 more source

Dynamics of the degradation of ubiquitinated proteins by proteasomes and autophagy: association with sequestosome 1/p62.

The Journal of biological chemistry, 2011
Proteotoxicity resulting from accumulation of damaged/unwanted proteins contributes prominently to cellular aging and neurodegeneration. Proteasomal removal of these proteins upon covalent polyubiquitination is highly regulated. Recent reports proposed a role for autophagy in clearance of diffuse ubiquitinated proteins delivered by p62/SQSTM1. Here, we
Natura, Myeku, Maria E, Figueiredo-Pereira   +1 more
openaire   +1 more source

Correcting CFTR folding defects by small-molecule correctors to cure cystic fibrosis [PDF]

, 2017
Pharmacological intervention to treat the lethal genetic disease cystic fibrosis has become reality, even for the severe, most common folding mutant F508del CFTR. CFTR defects range from absence of the protein, misfolding that leads to degradation rather
Sub Cellular Protein Chemistry, Mijnders, Marjolein, Marjolein Mijnders, Ineke Braakman, Bertrand Kleizen, Braakman, Ineke, Cellular Protein Chemistry, Kleizen, Bertrand   +7 more
core   +1 more source

Repeated Moderate and Severe Heat Exposure Has Divergent Effects on Skeletal Muscle Mitochondrial, Proteostatic and Neuromuscular Outcomes in Mice

Acta Physiologica, Volume 242, Issue 10, October 2026.
ABSTRACT Aim Repeated heat exposure may promote adaptive remodeling or cumulative tissue burden depending on thermal dose, but its graded molecular and functional consequences during recovery remain unclear. We examined whether repeated moderate (39°C) and severe (41°C) whole‐body hyperthermia produce distinct skeletal muscle trajectories involving ...
Cansu Yakin, Cihan Suleyman Erdogan, Fatma Ozge Tuncel, Yunus Kosif, Bayram Yilmaz   +4 more
wiley   +1 more source

Non-Contiguous Protein Recombination [PDF]

, 2013
Swapping sequence elements among related proteins can produce chimeric proteins with novel behaviors and improved properties such as enhanced stability. Although homologous mutations are much more conservative than random mutations, chimeras of distantly-
Smith, Matthew Alexander
core   +1 more source

Mitochondrial Dysfunction Unravels the Potential Molecular Link Between Night Shift Work‐Related Circadian Disruption and Elevated Blood Pressure in Human and Mouse Models

Advanced Science, Volume 13, Issue 52, 18 September 2026.
This diagram illustrates that night shift work disrupts circadian clock genes (like CLOCK, BMAL1) in both humans and mice. This disruption leads to mitochondrial dysfunction (imbalanced fusion/fission proteins) and increased oxidative stress, which is identified as the primary mechanism ultimately causing elevated blood pressure.
Zhaoqiang Jiang, Yifan Dou, Yingnan Lei, Shuang Liu, Jialin Zhou, Jiaping Li, Huadong Xu, Lingfang Feng, Yongxin Li, Chuyan Zhang, Tao Li, Jianfei Wang, Xing Zhang, Xinran Wang, Luyao Liu, Jingjing Zhang, Jianlin Lou   +16 more
wiley   +1 more source

Calcium as a crucial cofactor for low density lipoprotein receptor folding in the endoplasmic reticulum [PDF]

, 2010
The family of low density lipoprotein (LDL) receptors mediate uptake of a plethora of ligands from the circulation and couple this to signaling, thereby performing a crucial role in physiological processes including embryonic development, cancer ...
Sub Cellular Protein Chemistry, Pena, F., van Zadelhoff, G., Braakman, L.J., Cellular Protein Chemistry, Dep Scheikunde, Jansens, A.   +6 more
core   +2 more sources

Microplastics‐Induced Gut Microbiota Dysbiosis Accelerates Alzheimer's‐Like Pathology and Cognitive Decline via the Gut–Brain Axis

Advanced Science, Volume 13, Issue 50, 7 September 2026.
Microplastics (MPs) breach the gut‐brain axis by triggering taurine‐depleting microbiota dysbiosis that accelerates Alzheimer‐like pathology in 5XFAD mice. Taurine supplementation normalizes autophagy, microglial quiescence, and cognition, and plasma taurine inversely tracks cognitive decline in ADNI participants, revealing a readily translatable ...
Zifeng Wu, Jiarong Yang, Miaoxuan Zhang, Yi Li, Zhuling Tu, Ji Wang, Jin‐Tai Yu, Kun Guo, Rongcan Luo   +8 more
wiley   +1 more source