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Institution

Mitsubishi

CompanyTokyo, Japan
About: Mitsubishi is a company organization based out in Tokyo, Japan. It is known for research contribution in the topics: Layer (electronics) & Signal. The organization has 53115 authors who have published 54821 publications receiving 870150 citations. The organization is also known as: Mitsubishi Group of Companies & Mitsubishi Companies.


Papers
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Journal ArticleDOI
TL;DR: Ca2+ is likely to be functionally important in the control of mitochondrial dynamics through regulation of Drp1 phosphorylation in neurons and other cell types, suggesting that CaMKIα is a widely expressed protein kinase.
Abstract: Mitochondria are dynamic organelles that frequently move, divide, and fuse with one another to maintain their architecture and functions. However, the signaling mechanisms involved in these processes are still not well characterized. In this study, we analyze mitochondrial dynamics and morphology in neurons. Using time-lapse imaging, we find that Ca2+ influx through voltage-dependent Ca2+ channels (VDCCs) causes a rapid halt in mitochondrial movement and induces mitochondrial fission. VDCC-associated Ca2+ signaling stimulates phosphorylation of dynamin-related protein 1 (Drp1) at serine 600 via activation of Ca2+/calmodulin-dependent protein kinase Iα (CaMKIα). In neurons and HeLa cells, phosphorylation of Drp1 at serine 600 is associated with an increase in Drp1 translocation to mitochondria, whereas in vitro, phosphorylation of Drp1 results in an increase in its affinity for Fis1. CaMKIα is a widely expressed protein kinase, suggesting that Ca2+ is likely to be functionally important in the control of mitochondrial dynamics through regulation of Drp1 phosphorylation in neurons and other cell types.

400 citations

Journal ArticleDOI
TL;DR: The production of mice that lack Peg10 indicates that Peg10 is critical for mouse parthenogenetic development and provides the first direct evidence of an essential role of an evolutionarily conserved retrotransposon-derived gene in mammalian development.
Abstract: By comparing mammalian genomes, we and others have identified actively transcribed Ty3/gypsy retrotransposon-derived genes with highly conserved DNA sequences and insertion sites1,2,3,4,5,6. To elucidate the functions of evolutionarily conserved retrotransposon-derived genes in mammalian development, we produced mice that lack one of these genes, Peg10 (paternally expressed 10)1,2,3,7, which is a paternally expressed imprinted gene on mouse proximal chromosome 6. The Peg10 knockout mice showed early embryonic lethality owing to defects in the placenta. This indicates that Peg10 is critical for mouse parthenogenetic development and provides the first direct evidence of an essential role of an evolutionarily conserved retrotransposon-derived gene in mammalian development.

399 citations

Journal ArticleDOI
TL;DR: It is reported that p35 can be cleaved to p25 both in vitro and in vivo by calpain, suggesting a role of the cleavage in neuronal cell death.

395 citations

Journal ArticleDOI
TL;DR: The amino acid sequence of TPKI is presented, which is identical to glycogen synthase kinase 3β (GSK3β), and it is found that TPKI activity was inseparable from GSK3 activity throughout the purification procedure.

393 citations

Journal ArticleDOI
TL;DR: PRMT1 knockdown led to a decrease in oxidative-stress-induced apoptosis depending on the PI3K-Akt signaling pathway, and predicted a role for arginine methylation as an inhibitory modification against Akt-mediated phosphorylation.

390 citations


Authors

Showing all 53117 results

NameH-indexPapersCitations
Thomas S. Huang1461299101564
Kazunari Domen13090877964
Kozo Kaibuchi12949360461
Yoshimi Takai12268061478
William T. Freeman11343269007
Tadayuki Takahashi11293257501
Takashi Saito112104152937
H. Vincent Poor109211667723
Qi Tian96103041010
Andreas F. Molisch9677747530
Takeshi Sakurai9549243221
Akira Kikuchi9341228893
Markus Gross9158832881
Eiichi Nakamura9084531632
Michael Wooldridge8754350675
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Performance
Metrics
No. of papers from the Institution in previous years
YearPapers
20231
20222
2021199
2020310
2019389
2018422