Zobrazeno 1 - 10
of 32
pro vyhledávání: '"Hiroharu Arakawa"'
Autor:
Hidehito Kotani, Shinji Mizuarai, Takashi Yoshizumi, Takeshi Sagara, Toshihiro Sakamoto, Hiroharu Arakawa, Takumi Sakai, Jian Jiang, Tadahiro Nambu, Hiroko Oki, Kazuhiro Fukasawa, Ikuko Takahashi-Suzuki, Hiraku Itadani, Kazunori Yamanaka, Junko Ohtani, Naoki Kaneko, Toshifumi Kimura, Makiko Kobayashi, Toshihide Nishibata, Tsuyoshi Arai, Megumu Okada, Yoshikazu Iwasawa, Hiroshi Hirai
Supplementary Figure 4 from Small-molecule inhibition of Wee1 kinase by MK-1775 selectively sensitizes p53-deficient tumor cells to DNA-damaging agents
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::13fbd4990659e663b7dccb7e40258433
https://doi.org/10.1158/1535-7163.22486068
https://doi.org/10.1158/1535-7163.22486068
Autor:
Hidehito Kotani, Shinji Mizuarai, Takashi Yoshizumi, Takeshi Sagara, Toshihiro Sakamoto, Hiroharu Arakawa, Takumi Sakai, Jian Jiang, Tadahiro Nambu, Hiroko Oki, Kazuhiro Fukasawa, Ikuko Takahashi-Suzuki, Hiraku Itadani, Kazunori Yamanaka, Junko Ohtani, Naoki Kaneko, Toshifumi Kimura, Makiko Kobayashi, Toshihide Nishibata, Tsuyoshi Arai, Megumu Okada, Yoshikazu Iwasawa, Hiroshi Hirai
Wee1 is a tyrosine kinase that phosphorylates and inactivates CDC2 and is involved in G2 checkpoint signaling. Because p53 is a key regulator in the G1 checkpoint, p53-deficient tumors rely only on the G2 checkpoint after DNA damage. Hence, such tumo
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::6083f36a3d2a471a2a2ebf46afa829f9
https://doi.org/10.1158/1535-7163.c.6532227.v1
https://doi.org/10.1158/1535-7163.c.6532227.v1
Autor:
Hidehito Kotani, Shinji Mizuarai, Takashi Yoshizumi, Takeshi Sagara, Toshihiro Sakamoto, Hiroharu Arakawa, Takumi Sakai, Jian Jiang, Tadahiro Nambu, Hiroko Oki, Kazuhiro Fukasawa, Ikuko Takahashi-Suzuki, Hiraku Itadani, Kazunori Yamanaka, Junko Ohtani, Naoki Kaneko, Toshifumi Kimura, Makiko Kobayashi, Toshihide Nishibata, Tsuyoshi Arai, Megumu Okada, Yoshikazu Iwasawa, Hiroshi Hirai
Supplementary Figure 3 from Small-molecule inhibition of Wee1 kinase by MK-1775 selectively sensitizes p53-deficient tumor cells to DNA-damaging agents
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::96f3febe721d3504881be88ebdf1890e
https://doi.org/10.1158/1535-7163.22486071
https://doi.org/10.1158/1535-7163.22486071
Autor:
Hidehito Kotani, Shinji Mizuarai, Takashi Yoshizumi, Takeshi Sagara, Toshihiro Sakamoto, Hiroharu Arakawa, Takumi Sakai, Jian Jiang, Tadahiro Nambu, Hiroko Oki, Kazuhiro Fukasawa, Ikuko Takahashi-Suzuki, Hiraku Itadani, Kazunori Yamanaka, Junko Ohtani, Naoki Kaneko, Toshifumi Kimura, Makiko Kobayashi, Toshihide Nishibata, Tsuyoshi Arai, Megumu Okada, Yoshikazu Iwasawa, Hiroshi Hirai
Supplementary Figure 1 from Small-molecule inhibition of Wee1 kinase by MK-1775 selectively sensitizes p53-deficient tumor cells to DNA-damaging agents
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::24fe199219c306c270d9d95973603ade
https://doi.org/10.1158/1535-7163.22486077
https://doi.org/10.1158/1535-7163.22486077
Autor:
Hidehito Kotani, Shinji Mizuarai, Takashi Yoshizumi, Takeshi Sagara, Toshihiro Sakamoto, Hiroharu Arakawa, Takumi Sakai, Jian Jiang, Tadahiro Nambu, Hiroko Oki, Kazuhiro Fukasawa, Ikuko Takahashi-Suzuki, Hiraku Itadani, Kazunori Yamanaka, Junko Ohtani, Naoki Kaneko, Toshifumi Kimura, Makiko Kobayashi, Toshihide Nishibata, Tsuyoshi Arai, Megumu Okada, Yoshikazu Iwasawa, Hiroshi Hirai
Supplementary Figure 2 from Small-molecule inhibition of Wee1 kinase by MK-1775 selectively sensitizes p53-deficient tumor cells to DNA-damaging agents
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::c548c563bdee1d537f11e9305fc523c6
https://doi.org/10.1158/1535-7163.22486074.v1
https://doi.org/10.1158/1535-7163.22486074.v1
Autor:
Takashi Yoshizumi, Kazunori Yamanaka, Makiko Kobayashi, Tsuyoshi Arai, Hiraku Itadani, Yoshikazu Iwasawa, Hiroshi Hirai, Naoki Kaneko, Toshihide Nishibata, Megumu Okada, Shinji Mizuarai, Junko Ohtani, Takumi Sakai, Takeshi Sagara, Tadahiro Nambu, Toshihiro Sakamoto, Kazuhiro Fukasawa, Ikuko Takahashi-Suzuki, Jian Jiang, Toshifumi Kimura, Hiroharu Arakawa, Hiroko Oki, Hidehito Kotani
Publikováno v:
Molecular Cancer Therapeutics. 8:2992-3000
Wee1 is a tyrosine kinase that phosphorylates and inactivates CDC2 and is involved in G2 checkpoint signaling. Because p53 is a key regulator in the G1 checkpoint, p53-deficient tumors rely only on the G2 checkpoint after DNA damage. Hence, such tumo
Publikováno v:
Biochemical and Biophysical Research Communications. 299:669-675
The ABC half-transporter, ABCG2, is known to confer resistance to chemotherapeutic agents including indolocarbazole derivatives. MCF7 cells were introduced by either wild type ABCG2 (ABCG2-482R) or mutant ABCG2 (-482T), whose amino acid at position 4
Autor:
Susumu Nishimura, Seigo Kamiya, Atsushi Hirano, Yoshiaki Monden, Masao Tsukamoto, Hiroharu Arakawa, Mayumi Futamura
Publikováno v:
Oncogene. 20:6724-6730
To search for anti-cancer agents, a screening system for Ras signal inhibitors was developed using a NIH3T3 cell line with an introduced reporter gene which is controlled by the Ras-responsive element (RRE). With this screening system, malolactomycin
Autor:
Mitsuru Ohkubo, Hiroharu Arakawa, Hiroshi Kawamoto, Tomoko Yoshinari, Hiroyuki Suda, Masato Nakano, Hajime Morishima, Susumu Nishimura, Teruki Honma, Teruyuki Nishimura
Publikováno v:
Bioorganic & Medicinal Chemistry Letters. 10:419-422
A new indolocarbazole compound, NB-506 (1), modified at the glucose group yielded a beta-D-glucopyranoside, J-107,088 (2), which showed potent anticancer activity. A beta-D-ribofuranoside, J-109,534 (3), was found to be 6 times more potent than J-107
Autor:
Hiroyuki Suda, Teruyuki Nishimura, Ikuko Nishimura, Teruki Honma, Tomoko Yoshinari, Hiroharu Arakawa, Mitsuru Ohkubo, Hajime Morishima, Susumu Nishimura, Satoru Ito
Publikováno v:
Bioorganic & Medicinal Chemistry Letters. 9:3307-3312
In the course of a study of 6-N-amino-substituted analogues of NB-506 (1), a more potent anticancer drug, J-109,404 (2), in which the formyl group of NB-506 was replaced with a 1,3-dihydroxypropane group, was reported. A study of further modification