ER stress and diseases
By Hiderou Yoshida. The FEBS Journal, 2007
1,128 citations recorded by the source corpus.
Subfields: Cell Biology, Epidemiology, Molecular Biology
View Paper: https://www.semanticscholar.org/paper/3ef615b4303e7af4ea1421db959bab2138ddf886
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Citations in the corpus
- Protein quality control in the early secretory pathway (2008, background): “The players, mechanisms and physiopathologic implications of this process (ER-associated degradation, ERAD) remain a hot topic in molecular cell biology (Yoshida, 2007).”
- Insight into nanoparticle cellular uptake and intracellular targeting (2014, neutral): “ER stress can lead to apoptosis that has been a cause of heart diseases (cardiac hypertrophy, degeneration of cardiomyocytes), liver diseases, neurodegenerative diseases, and diabetes [168,169].”
- The C/EBP Homologous Protein (CHOP) Transcription Factor Functions in Endoplasmic Reticulum Stress-Induced Apoptosis and Microbial Infection (2019, background): “Using the survival pathway, cells conquer such disadvantageous effects and maintain homeostasis through the UPR, inhibiting the transcription of mRNA, enhancing the folding capacity of the ER, and ERAD (ER-assisted degradation) to restore homeostasis (7).”
- ER stress: Autophagy induction, inhibition and selection (2015, background): “Finally, programmed cell execution is initiated when stress exceeds a given threshold and the ER is so severely impaired that compensatory mechanisms are no longer able to sustain its function.(6,7) Although ER stress and autophagy can function independently, they share a number of common features i”