Docosahexaenoic acid enhances methylmercury-induced endoplasmic reticulum stress and cell death and eicosapentaenoic acid potentially attenuates these effects in mouse embryonic fibroblasts

2019 ◽  
Vol 306 ◽  
pp. 35-42 ◽  
Author(s):  
Yasukazu Takanezawa ◽  
Ryosuke Nakamura ◽  
Miho Hamaguchi ◽  
Kanae Yamamoto ◽  
Yuka Sone ◽  
...  
Keyword(s):  
Endoplasmic Reticulum ◽  
Cell Death ◽  
Docosahexaenoic Acid ◽  
Endoplasmic Reticulum Stress ◽  
Eicosapentaenoic Acid ◽  
Mouse Embryonic Fibroblasts ◽  
Embryonic Fibroblasts

scholarly journals Endoplasmic Reticulum Stress-induced Death of Mouse Embryonic Fibroblasts Requires the Intrinsic Pathway of Apoptosis

2007 ◽  
Vol 282 (19) ◽  
pp. 14132-14139 ◽  
Author(s):  
Ali Masud ◽  
Alexander Mohapatra ◽  
Saquib A. Lakhani ◽  
Anthony Ferrandino ◽  
Razqallah Hakem ◽  
...  
Keyword(s):  
Endoplasmic Reticulum ◽  
Endoplasmic Reticulum Stress ◽  
Intrinsic Pathway ◽  
Mouse Embryonic Fibroblasts ◽  
Embryonic Fibroblasts

p62/sequestosome 1 attenuates methylmercury-induced endoplasmic reticulum stress in mouse embryonic fibroblasts

2021 ◽  
Author(s):  
Yasukazu Takanezawa ◽  
Ryosuke Nakamura ◽  
Takuro Sugimoto ◽  
Yuka Ohshiro ◽  
Shimpei Uraguchi ◽  
...  
Keyword(s):  
Endoplasmic Reticulum ◽  
Endoplasmic Reticulum Stress ◽  
Mouse Embryonic Fibroblasts ◽  
Embryonic Fibroblasts ◽  
Sequestosome 1

CUX1 controls endoplasmic reticulum stress and autophagy related cell death

2016 ◽  
Vol 54 (12) ◽  
pp. 1343-1404
Author(s):  
G Metzger ◽  
P Di Fazio ◽  
DK Bartsch ◽  
T Gress ◽  
TT Wissniowski
Keyword(s):  
Endoplasmic Reticulum ◽  
Cell Death ◽  
Endoplasmic Reticulum Stress ◽  
Related Cell

A novel transmembrane protein defines the endoplasmic reticulum stress-induced cell death pathway

2017 ◽  
Vol 486 (1) ◽  
pp. 149-155 ◽  
Author(s):  
Tomoya Tamaki ◽  
Kenta Kamatsuka ◽  
Taku Sato ◽  
Shuntaro Morooka ◽  
Kosuke Otsuka ◽  
...  
Keyword(s):  
Endoplasmic Reticulum ◽  
Cell Death ◽  
Endoplasmic Reticulum Stress ◽  
Transmembrane Protein ◽  
Cell Death Pathway

scholarly journals Mammalian E4 Is Required for Cardiac Development and Maintenance of the Nervous System

2005 ◽  
Vol 25 (24) ◽  
pp. 10953-10964 ◽  
Author(s):  
Chie Kaneko-Oshikawa ◽  
Tadashi Nakagawa ◽  
Mitsunori Yamada ◽  
Hiroo Yoshikawa ◽  
Masaki Matsumoto ◽  
...  
Keyword(s):  
Endoplasmic Reticulum ◽  
Endoplasmic Reticulum Stress ◽  
Cardiac Muscle ◽  
Cardiac Development ◽  
Physiological Function ◽  
Embryonic Fibroblasts ◽  
Adult Mice ◽  
Developing Heart ◽  
Ubiquitin Conjugation ◽  
Spinocerebellar Neurons

ABSTRACT Ubiquitin conjugation typically requires three classes of enzyme: E1, E2, and E3. A fourth type of enzyme (E4), however, was recently shown to be required for the degradation of certain types of substrate in yeast. We previously identified UFD2a (also known as E4B) as an E4 in mammals. UFD2a is exclusively expressed in cardiac muscle during mouse embryonic development, but it is abundant in neurons of adult mice and is implicated in the pathogenesis of neurodegenerative disease. The precise physiological function of this enzyme has remained largely unknown, however. Here, we show that mice lacking UFD2a die in utero, manifesting marked apoptosis in the developing heart. Polyubiquitylation activity for an E4 substrate was greatly reduced in Ufd2a −/− mouse embryonic fibroblasts. Furthermore, Ufd2a +/− mice displayed axonal dystrophy in the nucleus gracilis, as well as degeneration of Purkinje cells accompanied by endoplasmic reticulum stress. These animals also developed a neurological disorder. UFD2a thus appears to be essential for the development of cardiac muscle, as well as for the protection of spinocerebellar neurons from degeneration induced by endoplasmic reticulum stress.

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