Tyk2 mutation homologous to V617F Jak2 is not found in essential thrombocythaemia, although it induces constitutive signaling and growth factor independence

Kotaro Shide; Kazuya Shimoda; Kenjirou Kamezaki; Haruko Kakumitsu; Takashi Kumano; Akihiko Numata; Fumihiko Ishikawa; Katsuto Takenaka; Ken Yamamoto; Tadashi Matsuda; Mine Harada

doi:10.1016/j.leukres.2006.11.003

Tyk2 mutation homologous to V617F Jak2 is not found in essential thrombocythaemia, although it induces constitutive signaling and growth factor independence

Kotaro Shide, Kazuya Shimoda, Kenjirou Kamezaki, Haruko Kakumitsu, Takashi Kumano, Akihiko Numata, Fumihiko Ishikawa, Katsuto Takenaka, Ken Yamamoto, Tadashi Matsuda, Mine Harada

Center for Cellular and Molecular Medicine

Research output: Contribution to journal › Article › peer-review

10 Citations (Scopus)

Abstract

A single somatic mutation, V617F, in the pseudokinase domain of the Jak2 is the primary cause of many chronic myeloproliferative diseases. As valine 617 of Jak2 is conserved as valine 678 of Tyk2, we examined the effect of a homologous mutation in Tyk2 (V678F Tyk2) on cell growth. V678F Tyk2 augmented the transcriptional activity of Stat3 and Stat5. The expression of V678F Tyk2 in Ba/F3 cells induced autonomous cell growth and showed hyper-responsiveness to IL-3. Although V678F Tyk2 might cause MPD, no cases of ET patients lacking the V617F Jak2 mutation harbored the Tyk2 mutation.

Original language	English
Pages (from-to)	1077-1084
Number of pages	8
Journal	Leukemia Research
Volume	31
Issue number	8
DOIs	https://doi.org/10.1016/j.leukres.2006.11.003
Publication status	Published - Aug 2007

All Science Journal Classification (ASJC) codes

Hematology
Oncology
Cancer Research

UN SDGs

This output contributes to the following UN Sustainable Development Goals (SDGs)

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10.1016/j.leukres.2006.11.003

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Shide, K., Shimoda, K., Kamezaki, K., Kakumitsu, H., Kumano, T., Numata, A., Ishikawa, F., Takenaka, K., Yamamoto, K., Matsuda, T., & Harada, M. (2007). Tyk2 mutation homologous to V617F Jak2 is not found in essential thrombocythaemia, although it induces constitutive signaling and growth factor independence. Leukemia Research, 31(8), 1077-1084. https://doi.org/10.1016/j.leukres.2006.11.003

Shide, K, Shimoda, K, Kamezaki, K, Kakumitsu, H, Kumano, T, Numata, A, Ishikawa, F, Takenaka, K, Yamamoto, K, Matsuda, T & Harada, M 2007, 'Tyk2 mutation homologous to V617F Jak2 is not found in essential thrombocythaemia, although it induces constitutive signaling and growth factor independence', Leukemia Research, vol. 31, no. 8, pp. 1077-1084. https://doi.org/10.1016/j.leukres.2006.11.003

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title = "Tyk2 mutation homologous to V617F Jak2 is not found in essential thrombocythaemia, although it induces constitutive signaling and growth factor independence",

abstract = "A single somatic mutation, V617F, in the pseudokinase domain of the Jak2 is the primary cause of many chronic myeloproliferative diseases. As valine 617 of Jak2 is conserved as valine 678 of Tyk2, we examined the effect of a homologous mutation in Tyk2 (V678F Tyk2) on cell growth. V678F Tyk2 augmented the transcriptional activity of Stat3 and Stat5. The expression of V678F Tyk2 in Ba/F3 cells induced autonomous cell growth and showed hyper-responsiveness to IL-3. Although V678F Tyk2 might cause MPD, no cases of ET patients lacking the V617F Jak2 mutation harbored the Tyk2 mutation.",

author = "Kotaro Shide and Kazuya Shimoda and Kenjirou Kamezaki and Haruko Kakumitsu and Takashi Kumano and Akihiko Numata and Fumihiko Ishikawa and Katsuto Takenaka and Ken Yamamoto and Tadashi Matsuda and Mine Harada",

note = "Funding Information: This work was supported in part by a Grant from the Nakamura Foundation and by Grants-in-Aid for Scientific Research (numbers 13218096 and 15390302) from the Ministry of Education, Culture, Sports, Science, and Technology of Japan. ",

year = "2007",

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doi = "10.1016/j.leukres.2006.11.003",

language = "English",

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T1 - Tyk2 mutation homologous to V617F Jak2 is not found in essential thrombocythaemia, although it induces constitutive signaling and growth factor independence

AU - Shide, Kotaro

AU - Shimoda, Kazuya

AU - Kamezaki, Kenjirou

AU - Kakumitsu, Haruko

AU - Kumano, Takashi

AU - Numata, Akihiko

AU - Ishikawa, Fumihiko

AU - Takenaka, Katsuto

AU - Yamamoto, Ken

AU - Matsuda, Tadashi

AU - Harada, Mine

N1 - Funding Information: This work was supported in part by a Grant from the Nakamura Foundation and by Grants-in-Aid for Scientific Research (numbers 13218096 and 15390302) from the Ministry of Education, Culture, Sports, Science, and Technology of Japan.

PY - 2007/8

Y1 - 2007/8

N2 - A single somatic mutation, V617F, in the pseudokinase domain of the Jak2 is the primary cause of many chronic myeloproliferative diseases. As valine 617 of Jak2 is conserved as valine 678 of Tyk2, we examined the effect of a homologous mutation in Tyk2 (V678F Tyk2) on cell growth. V678F Tyk2 augmented the transcriptional activity of Stat3 and Stat5. The expression of V678F Tyk2 in Ba/F3 cells induced autonomous cell growth and showed hyper-responsiveness to IL-3. Although V678F Tyk2 might cause MPD, no cases of ET patients lacking the V617F Jak2 mutation harbored the Tyk2 mutation.

AB - A single somatic mutation, V617F, in the pseudokinase domain of the Jak2 is the primary cause of many chronic myeloproliferative diseases. As valine 617 of Jak2 is conserved as valine 678 of Tyk2, we examined the effect of a homologous mutation in Tyk2 (V678F Tyk2) on cell growth. V678F Tyk2 augmented the transcriptional activity of Stat3 and Stat5. The expression of V678F Tyk2 in Ba/F3 cells induced autonomous cell growth and showed hyper-responsiveness to IL-3. Although V678F Tyk2 might cause MPD, no cases of ET patients lacking the V617F Jak2 mutation harbored the Tyk2 mutation.

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SN - 0145-2126

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JO - Leukemia Research

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Tyk2 mutation homologous to V617F Jak2 is not found in essential thrombocythaemia, although it induces constitutive signaling and growth factor independence

Abstract

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