Zobrazeno 1 - 10
of 119
pro vyhledávání: '"Shigemasa, Hanazawa"'
Autor:
Hikari Narabayashi, Chiharu Koma, Kazuaki Nakata, Mion Ikegami, Yusuke Nakanishi, Jun Ogihara, Masato Tsuda, Akira Hosono, Shigemasa Hanazawa, Kyoko Takahashi
Publikováno v:
Frontiers in Molecular Biosciences, Vol 9 (2022)
The intestine is inhabited by a large number of commensal bacteria that are immunologically non-self, potentially causing inflammation. However, in a healthy intestine, inflammation is strictly controlled at low levels to maintain homeostasis. We pre
Externí odkaz:
https://doaj.org/article/214176f620144540b28682d397f6aebf
Autor:
Kentaro Hosokawa, Ben D. MacArthur, Yoshiko Matsumoto Ikushima, Hirofumi Toyama, Yoshikazu Masuhiro, Shigemasa Hanazawa, Toshio Suda, Fumio Arai
Publikováno v:
Nature Communications, Vol 8, Iss 1, Pp 1-15 (2017)
Repeated cell divisions induce DNA damage in haematopoietic stem cells (HSC) and telomeres are sensitive to this damage. Here, the authors show in murine HSCs that the telomere binding protein POT1a inhibited the production of reactive oxygen species
Externí odkaz:
https://doaj.org/article/103e2c9006e24accbe1d6a3f00d0aa0c
Autor:
Yoshinori Ohno, Kyoko Suzuki-Takedachi, Shin'ichiro Yasunaga, Toshiaki Kurogi, Mimoko Santo, Yoshikazu Masuhiro, Shigemasa Hanazawa, Motoaki Ohtsubo, Kazuhito Naka, Yoshihiro Takihara
Publikováno v:
PLoS ONE, Vol 11, Iss 5, p e0155558 (2016)
Geminin regulates chromatin remodeling and DNA replication licensing which play an important role in regulating cellular proliferation and differentiation. Transcription of the Geminin gene is regulated via an E2F-responsive region, while the protein
Externí odkaz:
https://doaj.org/article/2c0e98ef86964895a4e0309e70097988
Autor:
Yutaka Sugi, Kyoko Takahashi, Kenta Kurihara, Kazuaki Nakata, Hikari Narabayashi, Yuji Hamamoto, Makoto Suzuki, Masato Tsuda, Shigemasa Hanazawa, Akira Hosono, Shuichi Kaminogawa
Publikováno v:
PLoS ONE, Vol 11, Iss 10, p e0164858 (2016)
Immune responses against gut microbiota should be minimized to avoid unnecessary inflammation at mucosal surface. In this study, we analyzed the expression patterns of Toll-interacting protein (Tollip), an inhibitor of TLRs and IL-1 family cytokine-r
Externí odkaz:
https://doaj.org/article/447abe66a8c24cd18016c9a4d3acd7b4
Autor:
Ryutarou Nakayama, Wataru Sakurai, Shigemasa Hanazawa, Yoshikazu Masuhiro, Risa Nakano, Azusa Miyamoto, Michitaka Oho
Publikováno v:
Journal of Biological Chemistry. 291:22650-22660
TIPE2 (TNF-α-induced protein 8-like 2) is a novel death effector domain protein and is a negative regulator of the innate and adaptive immune response. Although it has been demonstrated that caspase-8 contributes to the negative regulation of TIPE2,
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::6835eaa2cc0ac765bb2e48ea0d640a83
https://doi.org/10.1074/jbc.m116.733451
https://doi.org/10.1074/jbc.m116.733451
Publikováno v:
Bioscience, biotechnology, and biochemistry. 83(2)
Suppressor of cytokine signaling (SOCS) 2, a negative regulator of growth hormone (GH) and insulin-like growth factor 1 (IGF-1), which is associated with acromegaly and cancers, is a promising candidate molecule for treating various diseases. To faci
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::b67e94cddcdfdc6df728217a564483b2
https://pubmed.ncbi.nlm.nih.gov/30343638
https://pubmed.ncbi.nlm.nih.gov/30343638
Autor:
Toshio Suda, Kentaro Hosokawa, Fumio Arai, Yoshikazu Masuhiro, Ben D. MacArthur, Shigemasa Hanazawa, Yoshiko Matsumoto Ikushima, Hirofumi Toyama
Publikováno v:
Nature Communications, Vol 8, Iss 1, Pp 1-15 (2017)
Nature Communications
Nature Communications
Repeated cell divisions and aging impair stem cell function. However, the mechanisms by which this occurs are not fully understood. Here we show that protection of telomeres 1A (Pot1a), a component of the Shelterin complex that protects telomeres, im
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::a2cec92bb4c2eaa25e89c2feb70e0d67
https://eprints.soton.ac.uk/413651/
https://eprints.soton.ac.uk/413651/
Autor:
Masayoshi Soma, Kosuke Saito, Shigemasa Hanazawa, Takahiro Ueno, Kyoko Fujiwara, Hiroyuki Matsuda, Yoshikazu Masuhiro, Noboru Fukuda, Ken-ichi Shinohara
Publikováno v:
The International Journal of Biochemistry & Cell Biology. 66:112-120
Transforming growth factor-β1 (TGF-β1) is a potent induction factor for epithelial-mesenchymal transition (EMT). Mesenchymal-epithelial transition (MET), as the inverse process of EMT, has recently been reported to promote the induction of induced
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::f83dfdaf16637f77c27e55881847ad27
https://doi.org/10.1016/j.biocel.2015.07.011
https://doi.org/10.1016/j.biocel.2015.07.011
Autor:
Kentaro, Hosokawa, Ben D, Macarthur, Yoshiko, Ikushima, Hirofumi, Toyama, Yoshikazu, Masuhiro, Shigemasa, Hanazawa, Toshio, Suda, Fumio, Arai
Publikováno v:
[Rinsho ketsueki] The Japanese journal of clinical hematology. 58(8)
Repeated cell divisions induce DNA damage accumulation, which impairs stem cell function during aging. However, the general molecular mechanisms by which this occurs remain unclear. Herein, we show that the expression of protection of telomeres 1a (P
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=pmid________::86e19884befa14067035836bbd52e6f6
https://pubmed.ncbi.nlm.nih.gov/28883279
https://pubmed.ncbi.nlm.nih.gov/28883279
Autor:
Yutaka Sugi, Yusuke Nakanishi, Akira Hosono, Hikari Narabayashi, Tetsuro Kobayakawa, Shuichi Kaminogawa, Masato Tsuda, Kyoko Takahashi, Kazuaki Nakata, Shigemasa Hanazawa
Publikováno v:
The Journal of biological chemistry. 292(37)
The intestinal tract contains many commensal bacteria that modulate various physiological host functions. Dysbiosis of commensal bacteria triggers dysfunction of the intestinal epithelial barrier, leading to the induction or aggravation of intestinal
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::d0e7df9572db952085d58860bc712efe
https://pubmed.ncbi.nlm.nih.gov/28760826
https://pubmed.ncbi.nlm.nih.gov/28760826