Zobrazeno 1 - 10
of 52
pro vyhledávání: '"Tze Mun Loo"'
Autor:
Sho Sugawara, Ryo Okada, Tze Mun Loo, Hisamichi Tanaka, Kenichi Miyata, Masatomo Chiba, Hiroko Kawasaki, Kaoru Katoh, Shizuo Kaji, Yoshiro Maezawa, Koutaro Yokote, Mizuho Nakayama, Masanobu Oshima, Koji Nagao, Chikashi Obuse, Satoshi Nagayama, Keiyo Takubo, Akira Nakanishi, Masato T. Kanemaki, Eiji Hara, Akiko Takahashi
Publikováno v:
Communications Biology, Vol 5, Iss 1, Pp 1-13 (2022)
The levels of catalytic subunit of the RNaseH2 enzyme, RNAseH2A, decrease during senescence promoting nucleotide accumulation and a senescence-associated secretory phenotype.
Externí odkaz:
https://doaj.org/article/c3317a7c0604439689709bd59c372b06
Autor:
Nanase Igarashi, Kenichi Miyata, Tze Mun Loo, Masatomo Chiba, Aki Hanyu, Mika Nishio, Hiroko Kawasaki, Hao Zheng, Shinya Toyokuni, Shunsuke Kon, Keiji Moriyama, Yasuyuki Fujita, Akiko Takahashi
Publikováno v:
Nature Communications, Vol 13, Iss 1, Pp 1-11 (2022)
Ras mutations induce cell competition and cellular senescence to inhibit the proliferation of oncogenic mutated cells. Here the authors demonstrate that cellular senescence inhibits cell competition-induced elimination of oncogenic cells through HGF
Externí odkaz:
https://doaj.org/article/fefee5d3488848f18ec4630c02187177
Autor:
Masahiro Wakita, Akiko Takahashi, Osamu Sano, Tze Mun Loo, Yoshinori Imai, Megumi Narukawa, Hidehisa Iwata, Tatsuyuki Matsudaira, Shimpei Kawamoto, Naoko Ohtani, Tamotsu Yoshimori, Eiji Hara
Publikováno v:
Nature Communications, Vol 11, Iss 1, Pp 1-13 (2020)
Senescent cells can influence the tumour microenvironment by secreting immunomodulatory factors and are thus a therapeutic target. Here, the authors identify a compound that degrades BET leading to DNA damage and activation of autophagy and a reducti
Externí odkaz:
https://doaj.org/article/cd78cc2a032e468c95cf625f4e739929
Autor:
Tomoka Misawa, Kazuhiro Hitomi, Kenichi Miyata, Yoko Tanaka, Risa Fujii, Masatomo Chiba, Tze Mun Loo, Aki Hanyu, Hiroko Kawasaki, Hisaya Kato, Yoshiro Maezawa, Koutaro Yokote, Asako J. Nakamura, Koji Ueda, Nobuo Yaegashi, Akiko Takahashi
Publikováno v:
International Journal of Molecular Sciences, Vol 24, Iss 3, p 2421 (2023)
Senescent cells exhibit several typical features, including the senescence-associated secretory phenotype (SASP), promoting the secretion of various inflammatory proteins and small extracellular vesicles (EVs). SASP factors cause chronic inflammation
Externí odkaz:
https://doaj.org/article/135f62b375f44a1abe07d20f75811edb
Publikováno v:
Cells, Vol 11, Iss 12, p 1958 (2022)
Cancer cells exhibit the unique characteristics of high proliferation and aberrant DNA damage response, which prevents cancer therapy from effectively eliminating them. The machinery required for telomere maintenance, such as telomerase and the alter
Externí odkaz:
https://doaj.org/article/5fcf279be8fb400fa82a112e2796eedd
Autor:
Akiko Takahashi, Tze Mun Loo, Ryo Okada, Fumitaka Kamachi, Yoshihiro Watanabe, Masahiro Wakita, Sugiko Watanabe, Shimpei Kawamoto, Kenichi Miyata, Glen N. Barber, Naoko Ohtani, Eiji Hara
Publikováno v:
Nature Communications, Vol 9, Iss 1, Pp 1-12 (2018)
Activation of DNA damage response induces the acquisition of senescence-associated secretory phenotype (SASP) in senescent cells, but precise mechanisms remain unclear. Here, the authors show that the cytoplasmic accumulation of nuclear DNA activated
Externí odkaz:
https://doaj.org/article/46c6acdb2be24972a182358d788f7bc6
Autor:
Naoko Ohtani, Eiji Hara, Makoto Arita, Masanobu Oshima, Shuh Narumiya, Tomohiro Aoki, Makoto M. Taketo, Koichi Watashi, Miho Kumagai, Masaru Nakamura, Takayuki Ozawa, Yukihiko Sugimoto, Tomoaki Koga, Atsushi Iwama, Yaeko Nakajima-Takagi, Yuriko Arai, Hiroaki Kanda, Shin Yoshimoto, Yoshihiro Watanabe, Fumitaka Kamachi, Tze Mun Loo
Supplementary Figure S6. Histopathology analysis of liver cancer.
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::1f910e38b84dc0b308e96ddc1e3f7e48
https://doi.org/10.1158/2159-8290.22532110.v1
https://doi.org/10.1158/2159-8290.22532110.v1
Publikováno v:
International Journal of Molecular Sciences, Vol 21, Iss 10, p 3720 (2020)
DNA damage, caused by various oncogenic stresses, can induce cell death or cellular senescence as an important tumor suppressor mechanism. Senescent cells display the features of a senescence-associated secretory phenotype (SASP), secreting inflammat
Externí odkaz:
https://doaj.org/article/e9b01196be094fd4bf0d30da4f18d32f
Autor:
Ryota Yamagishi, Fumitaka Kamachi, Masaru Nakamura, Shota Yamazaki, Tomonori Kamiya, Masaki Takasugi, Yi Cheng, Yoshiki Nonaka, Yoshimi Yukawa-Muto, Le Thi Thanh Thuy, Yohsuke Harada, Tatsuya Arai, Tze Mun Loo, Shin Yoshimoto, Tatsuya Ando, Masahiro Nakajima, Hayao Taguchi, Takamasa Ishikawa, Hisaya Akiba, Sachiko Miyake, Masato Kubo, Yoichiro Iwakura, Shinji Fukuda, Wei-Yu Chen, Norifumi Kawada, Alexander Rudensky, Susumu Nakae, Eiji Hara, Naoko Ohtani
Publikováno v:
Science Immunology. 7
研究グループは、肝臓に移行した腸内細菌叢の成分であるリポタイコ酸が、肝がん微小環境を変化させてがんの増殖進展を促進するSASP(Senescence-associated secretory phenotype、細胞老化随伴分泌
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::22dc685e477ecf77b1458daedaa42d75
https://doi.org/10.1126/sciimmunol.abl7209
https://doi.org/10.1126/sciimmunol.abl7209
Autor:
Akiko Takahashi, Masahiro Wakita, Shimpei Kawamoto, Tatsuyuki Matsudaira, Hidehisa Iwata, Osamu Sano, Tamotsu Yoshimori, Tze Mun Loo, Naoko Ohtani, Megumi Narukawa, Eiji Hara, Yoshinori Imai
Publikováno v:
Nature Communications, Vol 11, Iss 1, Pp 1-13 (2020)
Nature Communications
Nature Communications
Although cellular senescence acts primarily as a tumour suppression mechanism, the accumulation of senescent cells in vivo eventually exerts deleterious side effects through inflammatory/tumour-promoting factor secretion. Thus, the development of new
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::1559d8e5a341ce3d68b8f609bf090ff9
http://link.springer.com/article/10.1038/s41467-020-15719-6
http://link.springer.com/article/10.1038/s41467-020-15719-6