Zobrazeno 1 - 10
of 76
pro vyhledávání: '"Michio Nakaya"'
Autor:
Yuma Horii, Shoichi Matsuda, Chikashi Toyota, Takumi Morinaga, Takeo Nakaya, Soken Tsuchiya, Masaki Ohmuraya, Takanori Hironaka, Ryo Yoshiki, Kotaro Kasai, Yuto Yamauchi, Noburo Takizawa, Akiomi Nagasaka, Akira Tanaka, Hidetaka Kosako, Michio Nakaya
Publikováno v:
Nature Communications, Vol 14, Iss 1, Pp 1-19 (2023)
Heart fibrosis involves a feedback loop where stiffening increases fibrosis-related gene expression in myofibroblasts. Here authors reveal the mechanosensitive nuclear translocation of VGLL3, where it phase separates and promotes collagen production,
Externí odkaz:
https://doaj.org/article/3d91cd5901fb4a358a83f06efa607833
Autor:
Akiomi Nagasaka, Tsuyoshi Terawaki, Makoto Noda, Miyuki Takashima, Mika Fujino, Yuto Yamauchi, Shigeki Arawaka, Takeo Kato, Michio Nakaya
Publikováno v:
FEBS Open Bio, Vol 13, Iss 2, Pp 380-391 (2023)
During myocardial infarction (MI), cardiac cells at the infarcted area undergo cell death. In response, cardiac myofibroblasts, which are mainly differentiated from resident fibroblasts upon inflammation, produce extracellular matrix proteins such as
Externí odkaz:
https://doaj.org/article/8e3ca3d61f7940169494986694c1a8e6
Autor:
Yuya Yoshida, Naoya Matsunaga, Takaharu Nakao, Kengo Hamamura, Hideaki Kondo, Tomomi Ide, Hiroyuki Tsutsui, Akito Tsuruta, Masayuki Kurogi, Michio Nakaya, Hitoshi Kurose, Satoru Koyanagi, Shigehiro Ohdo
Publikováno v:
Nature Communications, Vol 12, Iss 1, Pp 1-17 (2021)
Alteration of circadian rhythms is often observed in patients with chronic kidney disease (CKD). Here, the authors show that CKD-induced dysfunction of the circadian clock increases the expression of G protein-coupled receptor 68 in circulating monoc
Externí odkaz:
https://doaj.org/article/003803f8997a470c8148526aae949ed1
Autor:
Akiomi Nagasaka, Chihiro Mogi, Hiroki Ono, Toshihide Nishi, Yuma Horii, Yuki Ohba, Koichi Sato, Michio Nakaya, Fumikazu Okajima, Hitoshi Kurose
Publikováno v:
Scientific Reports, Vol 7, Iss 1, Pp 1-11 (2017)
Abstract Myocardial infarction (MI) is an ischaemic heart condition caused by the occlusion of coronary arteries. Following MI, lactic acid from anaerobic glycolysis increases and infiltrating immune cells produce severe inflammation, which leads to
Externí odkaz:
https://doaj.org/article/79bdd7ecb0b44afb8eab5d5cabbfc604
Publikováno v:
Bio-Protocol, Vol 7, Iss 18 (2017)
In myocardial infarction (MI), a plenty of cardiomyocytes undergo necrosis and necroptosis due to the lack of oxygen and nutrients. The dead cardiomyocytes are promptly engulfed by phagocytes. When the dead cells are not engulfed, the noxious content
Externí odkaz:
https://doaj.org/article/c46157ad3f704121a3a0f730547f3e54
Publikováno v:
Bio-Protocol, Vol 7, Iss 18 (2017)
In myocardial infarction (MI), a number of cardiomyocytes undergo apoptosis. These apoptotic cardiomyocytes are promptly engulfed by phagocytes. If the dead cells are not engulfed, their noxious contents are released outside, resulting in induction o
Externí odkaz:
https://doaj.org/article/c70766eaf21c46cba2a9a7ff90d0151c
Publikováno v:
Journal of Pharmacological Sciences, Vol 122, Iss 1, Pp 1-9 (2013)
Abstract.: β-Arrestin-biased agonists are a new class of drugs with promising therapeutic effects. The molecular mechanisms of β-arrestin-biased agonists are still not completely identified. Here, we investigated the effect of angiotensin II (AngII
Externí odkaz:
https://doaj.org/article/400ebb6623b441b7acf74a4bef63ac17
Autor:
Ayaka Tobo, Masayuki Tobo, Takashi Nakakura, Masashi Ebara, Hideaki Tomura, Chihiro Mogi, Dong-Soon Im, Naoya Murata, Atsushi Kuwabara, Saki Ito, Hayato Fukuda, Mitsuhiro Arisawa, Satoshi Shuto, Michio Nakaya, Hitoshi Kurose, Koichi Sato, Fumikazu Okajima
Publikováno v:
PLoS ONE, Vol 10, Iss 6, p e0129334 (2015)
G protein-coupled receptor 4 (GPR4), previously proposed as the receptor for sphingosylphosphorylcholine, has recently been identified as the proton-sensing G protein-coupled receptor (GPCR) coupling to multiple intracellular signaling pathways, incl
Externí odkaz:
https://doaj.org/article/9cf59e4d2f3f49efb7bde40467363339
Publikováno v:
PLoS ONE, Vol 8, Iss 7, p e68351 (2013)
Beta-arrestins (β-arrestin1 and β-arrestin2) are known as cytosolic proteins that mediate desensitization and internalization of activated G protein-coupled receptors. In addition to these functions, β-arrestins have been found to work as adaptor
Externí odkaz:
https://doaj.org/article/5940f0f370e64881b0d3dd21a3ac20f1
Autor:
Akiomi Nagasaka, Tsuyoshi Terawaki, Makoto Noda, Miyuki Takashima, Mika Fujino, Yuto Yamauchi, Shigeki Arawaka, Takeo Kato, Michio Nakaya
Publikováno v:
FEBS Open Bio. 13:380-391