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FIP1L1 presence in FIP1L1-RARA or FIP1L1-PDGFRA differentially contributes to the pathogenesis of distinct types of leukemia

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Please use this identifier to cite or link to this item:http://hdl.handle.net/2115/59854

Title: FIP1L1 presence in FIP1L1-RARA or FIP1L1-PDGFRA differentially contributes to the pathogenesis of distinct types of leukemia
Authors: Iwasaki, Junko Browse this author
Kondo, Takeshi Browse this author →KAKEN DB
Darmanin, Stephanie Browse this author
Ibata, Makoto Browse this author
Onozawa, Masahiro Browse this author →KAKEN DB
Hashimoto, Daigo Browse this author
Sakamoto, Naoya Browse this author →KAKEN DB
Teshima, Takanori Browse this author →KAKEN DB
Keywords: FIP1L1
RARA
PDGFRA
Leukemia
Issue Date: Sep-2014
Publisher: Springer
Journal Title: Annals of Hematology
Volume: 93
Issue: 9
Start Page: 1473
End Page: 1481
Publisher DOI: 10.1007/s00277-014-2085-1
PMID: 24763514
Abstract: FIP1-like 1 (FIP1L1) is associated with two leukemogenic fusion genes: FIP1L1-retinoic acid receptor alpha (RARA) and FIP1L1-platelet-derived growth factor receptor alpha (PDGFRA). Analyses of a series of deletion mutants revealed that the FIP1 motif in FIP1L1-RARA plays a pivotal role in its homodimerization and transcriptional repressor activity. However, in FIP1L1-PDGFRA, the C-terminal PDGFRA portion possesses the ability of forming a homodimer by itself, making FIP1L1 dispensable for constitutive activation of this kinase. Both the full-length and the C-terminal PDGFRA portion of FIP1L1-PDGFRA could transform the IL-3-dependent hematopoietic cell line, BAF-B03. Moreover, when either the full-length or the C-terminal PDGFRA portion of FIP1L1-PDGFRA was introduced in these cells, they grew in the absence of IL-3. The cells having the C-terminal PDGFRA portion of FIP1L1-PDGFRA, however, were partially IL-3 dependent, whereas the cells having the full-length FIP1L1-PDGFRA became completely IL-3 independent for their growth. Taken together, these results show that FIP1L1 differentially contributes to the pathogenesis of distinct types of leukemia.
Rights: The final publication is available at link.springer.com
Type: article (author version)
URI: http://hdl.handle.net/2115/59854
Appears in Collections:医学院・医学研究院 (Graduate School of Medicine / Faculty of Medicine) > 雑誌発表論文等 (Peer-reviewed Journal Articles, etc)

Submitter: 近藤 健

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