Kyushu University Academic Staff Educational and Research Activities Database
List of Papers
AKIOMI NAGASAKA Last modified date:2020.06.01

Assistant Professor / Department of Pharmacology and Toxicology / Department of Pharmaceutical Health Care and Sciences / Faculty of Pharmaceutical Sciences

1. Takanori Hironaka, Tomoyuki Ueno, Kyosuke Mae, Chikashi Yoshimura, Takumi Morinaga, Yuma Horii, AKIOMI NAGASAKA, Hitoshi Kurose, Michio Nakaya., Drebrin is induced during myofibroblast differentiation and enhances the production of fibrosis-related genes, BBRC, 2020.05.
2. Horii Y, Nakaya M, Ohara H, Nishihara H, Watari K, NAGASAKA A, Nakaya T, Sugiura Y, Okuno T, Koga T, Tanaka A, Yokomizo T, Kurose H., Leukotriene B4 receptor 1 exacerbates inflammation following myocardial infarction., FASEB J., 2020.05.
3. Horii, Y., Matsuda, S., Watari, K., NAGASAKA, A., Kurose, H., Nakaya Michio, Phagocytosis Assay of Necrptotic Cells by Cardiac Myofibroblasts, Bio-protocol, 2017.10.
4. Horii, Y., Matsuda, S., Watari, K., NAGASAKA, A., Kurose, H, Nakaya, M, An Assay to Determine Phagocytosis of Apoptotic Cells by Cardiac Macrophages and Cardiac Myofibroblasts, Bio-protocol, 2017.10.
5. NAGASAKA, A., Mogi, C., Ono, H., Nishi, T., Horii, Y., Ohba, Y., Nakaya, M., Okajima, F., Kurose, H., The proton-sensing G protein-coupled receptor T-cell death-associated gene 8 (TDAG8) shows cardioprotective effects against myocardial infarction, Scientific Reports, 10.1038/s41598-017-07573-2, 2017.08, [URL].
6. Nakaya Michio, Watari Kenji, Tajima Mitsuru, Nakaya Takeo, Matsuda Shoichi, Ohara Hiroki, AKIOMI NAGASAKA, Horii Yuma, 他7名, Nagata Shigekazu, Hitoshi Kurose, Cardiac myofibroblast engulfment of dead cells facilitates recovery after myocardial infarction, J Clin Invest., 127, 383-401, 2017.01.
7. AKIOMI NAGASAKA, Ohba Yuki, Hitoshi Kurose, Nakaya Michio, Novel functions of GRK6 in macrophages by phosphorylating the non-GPCRs substrates, Macrophage,, 2, 2015.10, G protein-coupled receptor kinases (GRKs) were originally identified as molecules that phosphorylate G protein-coupled receptors (GPCRs) and play central roles in G protein-dependent physiological signalling. In addition, recent studies indicated that GRKs phosphorylate non-GPCR substrates and associate with a variety of proteins to regulate signal transduction. However, the involvement of GRKs in the physiological regulation of macrophages remains poorly understood. We identified GRK6 as a novel regulator of apoptotic cell clearance and inflammation in macrophages. GRK6 promotes the engulfment of apoptotic cells and is involved in a novel engulfment pathway that activates Rac1 independent of the two well-known engulfment pathways DOCK180/ELMO/Rac1 and GULP1/Rac1. We also revealed that GRK6 knockout mice spontaneously develop autoimmune-like diseases and exhibit impaired engulfment of senescent red blood cells and apoptotic cell clearance in the mouse spleen. In addition, we recently reported that GRK6 activates NF-κB signalling by the direct phosphorylation of IκBα, an inhibitor of NF-κB, in TNF-α-induced inflammation. Here we highlight the important roles of GRK6 in macrophages in tissue homeostasis and the immune response..
8. Yuki Ohba, Nakaya Michio, Kenji Watari, AKIOMI NAGASAKA, Hitoshi Kurose, GRK6 phosphorylates IkBa at Ser32/Ser36 and enhances TNF-a-induced inflammation, Biochemical and Biophysical Research Communications, 461, 2, 307-313, 2015.05, G protein-coupled receptor kinases (GRKs) comprise a family of seven serine/threonine kinases that phosphorylate agonist-activated G protein-coupled receptors (GPCRs). It has recently been reported that GRKs regulate GPCR-independent signaling through the phosphorylation of intracellular proteins. To date, several intracellular substrates for GRK2 and GRK5 have been reported. However, those for GRK6 are poorly understood. Here we identified IkBa, a negative regulator of NF-kB signaling, as a substrate for GRK6. GRK6 directly phosphorylated IkBa at Ser32/Ser36, and the kinase activity of GRK6 was required for the promotion of NF-kB signaling after TNF-a stimulation. Knockout of GRK6 in peritoneal macrophages
remarkably attenuated the transcription of inflammatory genes after TNF-a stimulation. In addition, we developed a bioluminescence resonance energy transfer (BRET) probe to monitor GRK6 activity. Using this probe, we revealed that the conformational change of GRK6 was induced by TNF-a. In summary, our study demonstrates that TNF-a induces GRK6 activation, and GRK6 promotes inflammatory responses through the phosphorylation of IkBa..
9. AKIOMI NAGASAKA, KAWANE KOHKI, YOSHIDA HIROKI, SHIGEKAZU NAGATA, Apaf-1-independent programmed cell death in mouse development, Cell Death Differ., 10.1038/cdd.2009.186, 17, 931-941, 2010.06.
10. MASAKI NAKAHARA, AKIOMI NAGASAKA, MASATO KOIKE, KOHKI KAWANE, YASUO UCHIYAMA, SHIGEKAZU NAGATA, Degradation of nuclear DNA by DNase II-like acid DNase in cortical fiber cells of mouse eye lens, FEBS, 274, 12, 3055-3064, 2007.06.