Results 101 to 110 of about 15,562 (187)
Respiratory syncytial virus (RSV) hijacks cholesterol or autophagy pathways to facilitate optimal replication. However, our understanding of the associated molecular mechanisms remains limited.
Lifeng Chen +9 more
doaj +1 more source
Muscle wasting in cancer cachexia: Mechanisms and the role of exercise
Abstract Cancer cachexia (CC) is a multifactorial disease marked by a severe and progressive loss of lean muscle mass and characterized further by inflammation and a negative energy/protein balance, ultimately leading to muscle atrophy and loss of muscle tissue.
Zoe P. Libramento +2 more
wiley +1 more source
YAP-increased autolysosome degradation is TEAD-dependent.
(A) TEAD1/3/4 was knocked down in normal and YAP-overexpressing MCF7 cells. Indicated cells were cultured for 6 h in normal medium (no treat), EBSS (ND) or EBSS +CQ. Total proteins were assayed by Western blotting.
Beibei Mao (712739) +7 more
core +1 more source
Mitochondrial dynamics and repair differences in two mouse models of Friedreich's ataxia
Abstract figure legend Differential mitochondrial remodelling in Friedreich's ataxia (FA)‐associated cardiomyopathy. Schematic summary of mitochondrial alterations in two mouse models of FA exhibiting distinct cardiac phenotypes. In cardiac/skeletal muscle‐specific MCK‐Cre frataxin knockout (FXN‐cKO) mice, which develop heart failure with reduced ...
Lili Salinas +5 more
wiley +1 more source
The IAP family member BRUCE regulates autophagosome–lysosome fusion
Autophagy has an important role in cellular homeostasis by degrading and recycling cytotoxic components. Ubiquitination is known to target cargoes for autophagy; however, key components of this pathway remain elusive.
Thomas Hoffmann +5 more
core +1 more source
This review highlights protein lactylation as a metabolic‐epigenetic regulator linking lactate reprogramming to programmed cell death. By modulating histone and non‐histone targets, lactylation reshapes cell fate decisions and represents a promising biomarker and therapeutic target in human diseases.
Yue Chen +8 more
wiley +1 more source
Polyploid giant cancer cells (PGCCs) arise in response to stress and play a critical role in therapy resistance and tumor dormancy. These cells can evade conventional treatments and later contribute to cancer relapse by generating progeny through nonmitotic, amitotic mechanisms.
Silvia Guil‐Luna +3 more
wiley +1 more source
Posttranslational Modifications of p62/SQSTM1 in Health and Disease
Schematic illustration of p62 as a posttranslational modifications (PTMs)‐programmed integrator in homeostasis, pathogenesis, and therapeutic targeting. (Left) Homeostasis: In physiological states, p62, through various PTMs such as phosphorylation, ubiquitination, and acetylation, coordinates essential cellular functions.
Weikai Wang +8 more
wiley +1 more source
TEM analysis of subcellular structures in both intact and 3 x 1s sonicated homogenates of PC3 cells.
(A–C) PC3 cells treated with DMSO showed only occasional autophagosome and autolysosome structures in both intact cells and homogenates. (D–F) PC3 cells treated with 2 µM GDC-0941 for 24 hours showed a slightly increased number of autophagosome and ...
Michael Degtyarev (516752) +2 more
core +1 more source
α‐Synuclein Promotes Atherosclerosis by Impairing Macrophage Autophagic Flux
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 +8 more
wiley +1 more source

