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905 results on '"Nishida, Eisuke"'

13. Identification of FAM53C as a cytosolic-anchoring inhibitory binding protein of the kinase DYRK1A

Author

70209914, Miyata, Yoshihiko, Nishida, Eisuke, 70209914, Miyata, Yoshihiko, and Nishida, Eisuke

Abstract

The protein kinase DYRK1A encoded in human chromosome 21 is the major contributor to the multiple symptoms observed in Down syndrome patients. In addition, DYRK1A malfunction is associated with various other neurodevelopmental disorders such as autism spectrum disorder. Here, we identified FAM53C with no hitherto known biological function as a novel suppressive binding partner of DYRK1A. FAM53C is bound to the catalytic protein kinase domain of DYRK1A, whereas DCAF7/WDR68, the major DYRK1A-binding protein, binds to the N-terminal domain of DYRK1A. The binding of FAM53C inhibited autophosphorylation activity of DYRK1A and its kinase activity to an exogenous substrate, MAPT/Tau. FAM53C did not bind directly to DCAF7/WDR68, whereas DYRK1A tethered FAM53C and DCAF7/WDR68 by binding concurrently to both of them, forming a tri-protein complex. DYRK1A possesses an NLS and accumulates in the nucleus when overexpressed in cells. Co-expression of FAM53C induced cytoplasmic re-localization of DYRK1A, revealing the cytoplasmic anchoring function of FAM53C to DYRK1A. Moreover, the binding of FAM53C to DYRK1A suppressed the DYRK1A-dependent nuclear localization of DCAF7/WDR68. All the results show that FAM53C binds to DYRK1A, suppresses its kinase activity, and anchors it in the cytoplasm. In addition, FAM53C is bound to the DYRK1A-related kinase DYRK1B with an Hsp90/Cdc37-independent manner. The results explain for the first time why endogenous DYRK1A is distributed in the cytoplasm in normal brain tissue. FAM53C-dependent regulation of the kinase activity and intracellular localization of DYRK1A may play a significant role in gene expression regulation caused by normal and aberrant levels of DYRK1A.

Published
2023

16. Beneficial innate signaling interference for antibacterial responses by a Toll-like receptor–mediated enhancement of the MKP-IRF3 axis

Author

Negishi, Hideo, Matsuki, Kosuke, Endo, Nobuyasu, Sarashina, Hana, Miki, Shoji, Matsuda, Atsushi, Fukazawa, Keiko, Taguchi-Atarashi, Naoko, Ikushima, Hiroaki, Yanai, Hideyuki, Nishio, Junko, Honda, Kenya, Fujioka, Yoichiro, Ohba, Yusuke, Noda, Tetsuo, Taniguchi, Shun'ichiro, Nishida, Eisuke, Zhang, Yongliang, Chi, Hongbo, Flavell, Richard A., and Taniguchi, Tadatsugu

Published
2013

37. Signalling through RHEB-1 mediates intermittent fasting-induced longevity in C. elegans

Author

Honjoh, Sakiko, Yamamoto, Takuya, Uno, Masaharu, and Nishida, Eisuke

Subjects
Caenorhabditis elegans -- Physiological aspects -- Genetic aspects -- Research -- Health aspects, Aging -- Physiological aspects -- Research -- Genetic aspects -- Health aspects, Insulin-like growth factor 1 -- Health aspects -- Genetic aspects -- Research -- Physiological aspects, Environmental issues, Science and technology, Zoology and wildlife conservation, Physiological aspects, Research, Genetic aspects, Health aspects
Abstract

Dietary restriction is the most effective and reproducible intervention to extend lifespan in divergent species (1). In mammals, two regimens of dietary restriction, intermittent fasting (IF) and chronic caloric restriction, have proven to extend lifespan and reduce the incidence of age-related disorders (2). An important characteristic of IF is that it can increase lifespan even when there is little or no overall decrease in calorie intake (2). The molecular mechanisms underlying IF-induced longevity, however, remain largely unknown. Here we establish an IF regimen that effectively extends the lifespan of Caenorhabditis elegans and show that the low molecular weight GTPase RHEB-1 has a dual role in lifespan regulation; RHEB-1 is required for the IF-induced longevity, whereas inhibition of RHEB-1 mimics the caloric-restriction effects. RHEB-1 exerts its effects in part by the insulin/insulin growth factor (IGF)-like signalling effect or DAF-16 in IF. Our analyses demonstrate that most fasting-induced upregulated genes require RHEB-1 function for their induction, and that RHEB-1 and TOR signalling are required for the fasting-induced downregulation of an insulin-like peptide, INS-7. These findings identify the essential role of signalling by RHEB-1 in IF-induced longevity and gene expression changes, and suggest a molecular link between the IF-induced longevity and the insulin/IGF-like signalling pathway., In an IF regimen, which has not been established in invertebrate model organisms, food is provided ad libitum to both control and experimental groups, but the experimental group is subjected [...]

Published
2009

48. The C. elegans p38 MAPK pathway regulates nuclear localization of the transcription factor SKN-1 in oxidative stress response

Author

Inoue, Hideki, Hisamoto, Naoki, Jae Hyung An, Oliveira, Riva P., Nishida, Eisuke, Blackwell, T. Keith, and Matsumoto, Kunihiro

Subjects
Mitogens -- Research, Protein kinases -- Research, Oxidative stress -- Research, Biological sciences
Abstract

The Caenorhabditis elegans PMK-1 p38 mitogen-activated protein kinase (MAPK) pathway regulates the oxidative stress response through the Cap-N-Collar transcription factor SKN-1. The results delineate the Caenorhabditis elegans p38 MAPK signaling pathway leading to the nucleus that responds to oxidative stress.

Published
2005

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