scholarly journals 4E-BP1 Protects Neurons from Misfolded Protein Stress and Parkinson's Disease Toxicity by Inducing the Mitochondrial Unfolded Protein Response

2020 ◽  
Vol 40 (45) ◽  
pp. 8734-8745
Author(s):  
Somasish Ghosh Dastidar ◽  
Michael T. Pham ◽  
Matthew B. Mitchell ◽  
Steven G. Yeom ◽  
Sarah Jordan ◽  
...  
2019 ◽  
Vol 111 (6) ◽  
pp. 161-168 ◽  
Author(s):  
Alexis Martinez ◽  
Nelida Lopez ◽  
Constanza Gonzalez ◽  
Claudio Hetz

2017 ◽  
Vol 26 (22) ◽  
pp. 4441-4450 ◽  
Author(s):  
Sabrina M Heman-Ackah ◽  
Raquel Manzano ◽  
Jeroen JM Hoozemans ◽  
Wiep Scheper ◽  
Rowan Flynn ◽  
...  

2011 ◽  
Vol 116 (4) ◽  
pp. 588-605 ◽  
Author(s):  
Arianna Bellucci ◽  
Laura Navarria ◽  
Michela Zaltieri ◽  
Elisa Falarti ◽  
Serena Bodei ◽  
...  

2007 ◽  
Vol 354 (3) ◽  
pp. 707-711 ◽  
Author(s):  
J.J.M. Hoozemans ◽  
E.S. van Haastert ◽  
P. Eikelenboom ◽  
R.A.I. de Vos ◽  
J.M. Rozemuller ◽  
...  

Cells ◽  
2020 ◽  
Vol 9 (11) ◽  
pp. 2495
Author(s):  
Cristine Alves da Costa ◽  
Wejdane El Manaa ◽  
Eric Duplan ◽  
Frédéric Checler

Parkinson’s disease (PD) is a multifactorial age-related movement disorder in which defects of both mitochondria and the endoplasmic reticulum (ER) have been reported. The unfolded protein response (UPR) has emerged as a key cellular dysfunction associated with the etiology of the disease. The UPR involves a coordinated response initiated in the endoplasmic reticulum that grants the correct folding of proteins. This review gives insights on the ER and its functioning; the UPR signaling cascades; and the link between ER stress, UPR activation, and physiopathology of PD. Thus, post-mortem studies and data obtained by either in vitro and in vivo pharmacological approaches or by genetic modulation of PD causative genes are described. Further, we discuss the relevance and impact of the UPR to sporadic and genetic PD pathology.


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