Zobrazeno 1 - 10
of 19
pro vyhledávání: '"Yoshihiko Kihara"'
Autor:
Tadaaki Inano, Marito Araki, Soji Morishita, Misa Imai, Yoshihiko Kihara, Maho Okuda, Yinjie Yang, Masafumi Ito, Satoshi Osaga, Hiroyuki Mano, Yoko Edahiro, Tomonori Ochiai, Kyohei Misawa, Yasutaka Fukuda, Jun Ando, Norio Komatsu
Publikováno v:
Scientific Reports, Vol 12, Iss 1, Pp 1-7 (2022)
Externí odkaz:
https://doaj.org/article/098c249009b9457ba2829d304a4b75a2
Autor:
Tadaaki Inano, Marito Araki, Soji Morishita, Misa Imai, Yoshihiko Kihara, Maho Okuda, Yinjie Yang, Masafumi Ito, Satoshi Osaga, Hiroyuki Mano, Yoko Edahiro, Tomonori Ochiai, Kyohei Misawa, Yasutaka Fukuda, Jun Ando, Norio Komatsu
Publikováno v:
Scientific Reports, Vol 11, Iss 1, Pp 1-11 (2021)
Abstract A subset of essential thrombocythemia (ET) cases are negative for disease-defining mutations on JAK2, MPL, and CALR and defined as triple negative (TN). The lack of recurrent mutations in TN-ET patients makes its pathogenesis ambiguous. Here
Externí odkaz:
https://doaj.org/article/a94cc6fdb69b4023a4cc0476b24bda89
Autor:
Misa Imai, Masafumi Ito, Kyohei Misawa, Maho Okuda, Yoko Edahiro, Tomonori Ochiai, Yoshihiko Kihara, Norio Komatsu, Jun Ando, Yinjie Yang, Soji Morishita, Satoshi Osaga, Yasutaka Fukuda, Tadaaki Inano, Marito Araki, Hiroyuki Mano
Publikováno v:
Scientific Reports
Scientific Reports, Vol 11, Iss 1, Pp 1-11 (2021)
Scientific Reports, Vol 11, Iss 1, Pp 1-11 (2021)
A subset of essential thrombocythemia (ET) cases are negative for disease-defining mutations on JAK2, MPL, and CALR and defined as triple negative (TN). The lack of recurrent mutations in TN-ET patients makes its pathogenesis ambiguous. Here, we scre
Autor:
Junichi Matsuo, Ryota Harai, Yoshihiko Kihara, Norio Komatsu, Tomoiku Takaku, Terumasa Umemoto, Seiichi Mori, Daniel G. Tenen, Toshio Suda, Motomi Osato, Eri Nakamura, Hitoshi Takizawa, Naomi Nakagata, Mineo Kurokawa, Norihiro Tada, Naoki Watanabe, Tomomasa Yokomizo, Akihiko Shimono, Tomohiko Sato
Publikováno v:
The Journal of Experimental Medicine
Hematopoietic stem cells (HSCs) and HSC-independent progenitors are generated from hemogenic endothelium. Yokomizo et al. show that Hlf expression distinguishes nascent HSCs from HSC-independent progenitors. HSC specification, regulated by the Evi-1/
Autor:
Riho Maeda, Nobutaka Hirano, Tsutomu Ishihara, Tsukasa Ichikawa, Yoshihiko Kihara, Nobukatsu Nemoto, Azusa Imaizumi, Mitsuru Haruki
Publikováno v:
Journal of Nanoscience and Nanotechnology. 17:5081-5089
Cell-specific gene delivery through conjugating targeting molecules to gene carriers is a promising strategy for gene therapy. Click chemistry is a convenient tool for such conjugations. We have developed siloxane-based amphiphilic polymers with alky
Autor:
Yosuke Mori, Misa Imai, Satoko Ogata, Mei Horino, Yo Mabuchi, Teppei Taguchi, Norio Komatsu, Soji Morishita, Yoshihiko Kihara, Syunpei Yoshikawa, Takehiro Suzuki, Nami Masubuchi, Yinjie Yang, Marito Araki, Chihiro Akazawa, Naoshi Domae, Yasutaka Fukuda, Akimichi Ohsaka, Motoyuki Shimonaka
Publikováno v:
Blood. 136:9-10
Mutant calreticulin (CALR) has been shown to play a causal role in the development of essential thrombocythemia (ET) and primary myelofibrosis (PMF) via activation of the thrombopoietin receptor MPL. The oncogenic property of mutant CALR originates f
Autor:
Misa Imai, Yinjie Yang, Masafumi Ito, Yoko Edahiro, Tomonori Ochiai, Tadaaki Inano, Satoshi Osaga, Norio Komatsu, Yasutaka Fukuda, Marito Araki, Soji Morishita, Akimichi Ohsaka, Kyohei Misawa, Yoshihiko Kihara, Maho Okuda
Publikováno v:
Blood. 136:27-28
Somatic mutations in JAK2, MPL, and CALR are found in approximately 80% of patients with essential thrombocythemia (ET), whereas the remaining patients are negative for disease-defining mutations and are defined as triple-negative (TN). Studies have
Autor:
Nami Masubuchi, Misa Imai, Marito Araki, Mai Nudejima, Yumi Hironaka, Yinjie Yang, Hiraku Takei, Akimichi Ohsaka, Yoko Edahiro, Yoshihiko Kihara, Norio Komatsu, Yoshihisa Mizukami, Erina Hayashi, Masato Koike
Publikováno v:
Leukemia. 34(2)
Studies have shown that mutant calreticulin (CALR) constitutively activates the thrombopoietin (TPO) receptor MPL and thus plays a causal role in the development of myeloproliferative neoplasms (MPNs). To further elucidate the molecular mechanism by
Autor:
Marito Araki, Nami Masubuchi, Norio Komatsu, Tadashi Matsuura, Yuta Ohira, Fumiko Nomura, Yoshihiko Kihara, Sota Kitazawa, Kaho Shioiri
Publikováno v:
Blood. 136:31-31
Iron incorporation through transferrin (Tf) and its receptor, TfR1, plays a critical role in erythropoiesis. We hypothesized that blockade of TfR1 may be a promising strategy to suppress erythrocytosis observed in polycythemia vera (PV). To examine t
Autor:
Yoko Edahiro, Marito Araki, Yumi Hironaka, Yoshihiko Kihara, Yoshitaka Sunami, Misa Imai, Norio Komatsu, Yinjie Yang, Yoshihisa Mizukami, Satoshi Osaga, Akimichi Ohsaka, Nami Masubuchi
Publikováno v:
Leukemia. 33(1)
Studies have previously shown that mutant calreticulin (CALR), found in a subset of patients with myeloproliferative neoplasms (MPNs), interacts with and subsequently promotes the activation of the thrombopoietin receptor (MPL). However, the molecula