scholarly journals Functional proteomics inCiona intestinalis: A breakthrough in the exploration of the molecular and cellular mechanism of ascidian development

2007 ◽  
Vol 236 (7) ◽  
pp. 1782-1789 ◽  
Author(s):  
Kazuo Inaba ◽  
Mamoru Nomura ◽  
Ayako Nakajima ◽  
Akiko Hozumi
2021 ◽  
Vol 2 (1) ◽  
pp. 100362
Author(s):  
Syed Nabeel-Shah ◽  
Jyoti Garg ◽  
Pata-Eting Kougnassoukou Tchara ◽  
Ronald E. Pearlman ◽  
Jean-Philippe Lambert ◽  
...  

2021 ◽  
Vol 63 ◽  
pp. 102061
Author(s):  
James M. Elmore ◽  
Brianna D. Griffin ◽  
Justin W. Walley

2019 ◽  
Vol 116 (50) ◽  
pp. 25322-25328 ◽  
Author(s):  
Yi Liu ◽  
Xiaopin Ma ◽  
Hisashi Fujioka ◽  
Jun Liu ◽  
Shengdi Chen ◽  
...  

Loss-of-function mutations in DJ-1 are associated with autosomal recessive early onset Parkinson’s disease (PD), yet the underlying pathogenic mechanism remains elusive. Here we demonstrate that DJ-1 localized to the mitochondria-associated membrane (MAM) both in vitro and in vivo. In fact, DJ-1 physically interacts with and is an essential component of the IP3R3-Grp75-VDAC1 complexes at MAM. Loss of DJ-1 disrupted the IP3R3-Grp75-VDAC1 complex and led to reduced endoplasmic reticulum (ER)-mitochondria association and disturbed function of MAM and mitochondria in vitro. These deficits could be rescued by wild-type DJ-1 but not by the familial PD-associated L166P mutant which had demonstrated reduced interaction with IP3R3-Grp75. Furthermore, DJ-1 ablation disturbed calcium efflux-induced IP3R3 degradation after carbachol treatment and caused IP3R3 accumulation at the MAM in vitro. Importantly, similar deficits in IP3R3-Grp75-VDAC1 complexes and MAM were found in the brain of DJ-1 knockout mice in vivo. The DJ-1 level was reduced in the substantia nigra of sporadic PD patients, which was associated with reduced IP3R3-DJ-1 interaction and ER-mitochondria association. Together, these findings offer insights into the cellular mechanism in the involvement of DJ-1 in the regulation of the integrity and calcium cross-talk between ER and mitochondria and suggests that impaired ER-mitochondria association could contribute to the pathogenesis of PD.


1992 ◽  
Vol 44 (12) ◽  
pp. 2409-2411 ◽  
Author(s):  
Toshiaki Emori ◽  
Yukio Hirata ◽  
Taihei Imai ◽  
Kazuki Ohta ◽  
Kazuo Kanno ◽  
...  

1985 ◽  
Vol 83 (1-2) ◽  
pp. 25-37 ◽  
Author(s):  
K. Strange ◽  
J. E. Phillips

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