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Identification of Flt3 internal tandem duplications downstream targets by high‐throughput immunoblotting protein array system
Author(s) -
Takahashi Shinichiro
Publication year - 2006
Publication title -
american journal of hematology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.456
H-Index - 105
eISSN - 1096-8652
pISSN - 0361-8609
DOI - 10.1002/ajh.20697
Subject(s) - fms like tyrosine kinase 3 , receptor tyrosine kinase , biology , mutation , haematopoiesis , tandem exon duplication , cancer research , tyrosine kinase , protein kinase domain , gene , microbiology and biotechnology , signal transduction , genetics , gene duplication , stem cell , mutant
The receptor tyrosine kinase Flt3 plays an important role in proliferation and survival of hematopoietic cells. Flt3 is the most frequently mutated gene (20–30%) in cases of acutemyeloid leukemia (AML). The majority of Flt3 mutations are internal tandem duplications (ITD) in the juxtamembrane domain of Flt3 receptor. This mutation results in the constitutive activation of STAT5 and Ras/mitogen‐activated protein kinase pathways, leading to the aberrant growth of AML cells. In this study, to better understand the mechanisms of Flt3‐ITD to the downstream pathways, a high‐throughput immunoblotting protein array system was employed. As a result, c‐Jun and c‐Raf were markedly induced, suggesting that these factors are functional downstream targets of Flt3‐ITD. Am. J. Hematol., 2006. © 2006 Wiley‐Liss, Inc.