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

研究成果: Contribution to journalArticle査読

9 被引用数 (Scopus)

抄録

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.

本文言語英語
ページ(範囲)1077-1084
ページ数8
ジャーナルLeukemia Research
31
8
DOI
出版ステータス出版済み - 8 2007

All Science Journal Classification (ASJC) codes

  • Hematology
  • Oncology
  • Cancer Research

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