Results 21 to 30 of about 166,195 (340)

Selective autophagy [PDF]

open access: yesCancer Science, 2021
AbstractWhile starvation‐induced autophagy is thought to randomly degrade cellular components, under certain circumstances autophagy selectively recognizes, sequesters, and degrades specific targets via autophagosomes. This process is called selective autophagy, and it contributes to cellular homeostasis by degrading specific soluble proteins ...
Mohammad Omar Faruk   +2 more
openaire   +2 more sources

NBR1: The archetypal selective autophagy receptor [PDF]

open access: hybridJournal of Cell Biology, 2022
NBR1 was discovered as an autophagy receptor not long after the first described vertebrate autophagy receptor p62/SQSTM1. Since then, p62 has currently been mentioned in >10,000 papers on PubMed, while NBR1 is mentioned in <350 papers. Nonetheless, evolutionary analysis reveals that NBR1, and likely also selective autophagy, was present ...
Nikoline Lander Rasmussen   +3 more
openalex   +4 more sources

The Roles of SQSTM1/p62 in Selective Autophagy and Oncogenic Signaling [PDF]

open access: goldInt J Mol Sci
Young-Jun Kim   +5 more
europepmc   +3 more sources

Selective autophagy as the basis of autophagy-based degraders [PDF]

open access: bronzeCell Chemical Biology, 2021
Degrader technologies, which enable the chemical knockdown of disease-causing proteins, are promising for drug discovery. After two decades of research, degraders using the ubiquitin-proteasome system (UPS) are currently in clinical trials. However, the UPS substrates are mainly limited to soluble proteins.
Daiki Takahashi, Hirokazu Arimoto
openalex   +3 more sources

Mechanisms of Selective Autophagy

open access: yesAnnual Review of Cell and Developmental Biology, 2021
Selective autophagy is the lysosomal degradation of specific intracellular components sequestered into autophagosomes, late endosomes, or lysosomes through the activity of selective autophagy receptors (SARs). SARs interact with autophagy-related (ATG)8 family proteins via sequence motifs called LC3-interacting region (LIR) motifs in vertebrates and ...
Lamark, Trond, Johansen, Terje
openaire   +5 more sources

Targeting Selective Autophagy as a Therapeutic Strategy for Viral Infectious Diseases

open access: yesFrontiers in Microbiology, 2022
Autophagy is an evolutionarily conserved lysosomal degradation system which can recycle multiple cytoplasmic components under both physiological and stressful conditions.
Yishan Liu   +7 more
doaj   +1 more source

Selective autophagy fine-tunes Stat92E activity by degrading Su(var)2-10/PIAS in <i>Drosophila</i> glia. [PDF]

open access: goldLife Sci Alliance
Vincze V   +9 more
europepmc   +2 more sources

Selective autophagy: Lysophagy [PDF]

open access: yesMethods, 2015
Autophagy is a bulk degradation system that is induced under stress conditions such as nutrient deprivation. Selective autophagy, including xenophagy and mitophagy, is believed to play important roles in the development of several diseases. Consequently, selective autophagy represents a potential therapeutic target. Recent work showed that the lysosome,
Junya, Hasegawa   +3 more
openaire   +2 more sources

Emerging mechanistic insights of selective autophagy in hepatic diseases

open access: yesFrontiers in Pharmacology, 2023
Macroautophagy (hereafter referred to as autophagy), a highly conserved metabolic process, regulates cellular homeostasis by degrading dysfunctional cytosolic constituents and invading pathogens via the lysosomal system.
Abdul Alim Al-Bari   +10 more
doaj   +1 more source

Selective Types of Autophagy [PDF]

open access: yesInternational Journal of Cell Biology, 2012
The focus of this special issue of the International Journal of Cell Biology is to underscore the recent developments in the field of macroautophagy and how this degradative pathway intersects with cellular metabolism, complex physiological functions, and human diseases. During the last decade, autophagy has become an expanding field in biomedical life
Fulvio Reggiori   +3 more
doaj   +3 more sources

Home - About - Disclaimer - Privacy