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

Research output: Contribution to journalArticle

9 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 languageEnglish
Pages (from-to)1077-1084
Number of pages8
JournalLeukemia Research
Volume31
Issue number8
DOIs
Publication statusPublished - Aug 2007

All Science Journal Classification (ASJC) codes

  • Hematology
  • Oncology
  • Cancer Research

Fingerprint Dive into the research topics of 'Tyk2 mutation homologous to V617F Jak2 is not found in essential thrombocythaemia, although it induces constitutive signaling and growth factor independence'. Together they form a unique fingerprint.

Cite this