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Up‐regulation of the T cell quiescence factor KLF2 in a leukaemic T‐cell line after expression of the inositol 5′‐phosphatase SHIP‐1
Author(s) -
GarcíaPalma Lizet,
Horn Stefan,
Haag Friedrich,
Diessenbacher Philip,
Streichert Thomas,
Mayr Georg W.,
Jücker Manfred
Publication year - 2005
Publication title -
british journal of haematology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.907
H-Index - 186
eISSN - 1365-2141
pISSN - 0007-1048
DOI - 10.1111/j.1365-2141.2005.05811.x
Subject(s) - jurkat cells , klf2 , microbiology and biotechnology , haematopoiesis , cell culture , biology , regulator , cell growth , signal transduction , gene expression , t cell , gene , immunology , stem cell , genetics , immune system
Summary Inositol 5′‐phosphatase SHIP‐1 (SHIP) is a negative regulator of signal transduction in haematopoietic cells. SHIP inactivation may be involved in the pathogenesis of leukaemia. An inducible expression system was combined with microarray analysis to identify target genes regulated by SHIP in the human T‐cell leukaemia cell line Jurkat. One gene identified was Krüppel‐like factor 2 ( KLF2 ), which was up‐regulated two to threefold at the RNA and protein level after the induced expression of SHIP. KLF2, a negative regulator of T cell proliferation, has been implicated in T cell quiescence. KLF2 or SHIP expression in Jurkat cells caused 45% or 60% reduction of proliferation, respectively. SHIP can up‐regulate KLF2 expression, implicating KLF2 in the SHIP‐mediated growth inhibition of a human leukaemic T‐cell line.