Fumihito Ueda on Muck Rack

Fumihito Ueda

As seen in: The Journal of Biological Chemistry
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Articles

Alpha-tocopherol attenuates the anti-tumor activity of crizotinib against cells transformed by NPM-ALK

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By Fumihito Ueda, Kenji Tago, Yuki Uchihara, Yosuke Nakazawa
| PLOS
Anaplastic large cell lymphomas (ALCL) are mainly characterized by harboring the fusion protein nucleophosmin-anaplastic lymphoma kinase (NPM-ALK). The ALK inhibitor, crizotinib specifically induced apoptosis in Ba/F3 cells expressing NPM-ALK by inhibiting the activation of NPM-ALK and its downstream molecule, signal transducer and activator of transcription factor 3 (STAT3).
Open in Who Shared Issue with article?

Three Tyrosine Residues in the Erythropoietin Receptor Are Essential for Janus Kinase 2 V617F Mutant-induced Tumorigenesis

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By Fumihito Ueda, Kenji Tago, Hiroomi Tamura, Megumi Funakoshi-Tago
| The Journal of Biological Chemistry Verified
The erythropoietin receptor (EpoR) regulates development of blood cells, and its full activation normally requires the cytokine erythropoietin (Epo). In the case of myeloproliferative neoplasms (MPN), Epo-independent signaling through EpoR can be caused by a point mutation, V617F, in the EpoR-interacting tyrosine kinase Janus kinase 2 (JAK2).
Open in Who Shared Issue with article?

Three Tyrosine Residues in the Erythropoietin Receptor Are Essential for Janus Kinase 2 V617F Mutant-Induced Tumorignesis

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By Fumihito Ueda, Kenji Tago, Hiroomi Tamura, Megumi Funakoshi-Tago
| The Journal of Biological Chemistry Verified
The erythropoietin receptor (EpoR) regulates development of blood cells, and its full activation normally requires the cytokine erythropoietin (Epo). In case of myeloproliferative neoplasms (MPN), Epo-independent signaling through EpoR can be caused by a point mutation, V617F, in the EpoR-interacting tyrosine kinase Janus kinase 2 (JAK2).
Open in Who Shared Issue with article?
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