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

Iwasaki, Junko; Kondo, Takeshi; Darmanin, Stephanie; Ibata, Makoto; Onozawa, Masahiro; Hashimoto, Daigo; Sakamoto, Naoya; Teshima, Takanori

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

Iwasaki, Junko; Kondo, Takeshi; Darmanin, Stephanie et al.

Annals of Hematology, 2014, 93(9), 1473-1481

Permalink : https://hdl.handle.net/2115/59854

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アクセス権	open access
URI	https://hdl.handle.net/2115/59854
タイトル	FIP1L1 presence in FIP1L1-RARA or FIP1L1-PDGFRA differentially contributes to the pathogenesis of distinct types of leukemia
著者	Iwasaki, Junko ; Kondo, Takeshi ; Darmanin, Stephanie ; Ibata, Makoto ; Onozawa, Masahiro ; Hashimoto, Daigo ; Sakamoto, Naoya ; Teshima, Takanori
著者名 Iwasaki, Junko
e-Rad_Researcher 70333606 著者名 Kondo, Takeshi
著者名 Darmanin, Stephanie
著者名 Ibata, Makoto
e-Rad_Researcher 70455632 著者名 Onozawa, Masahiro
著者名 Hashimoto, Daigo
e-Rad_Researcher 10334418 著者名 Sakamoto, Naoya
e-Rad_Researcher 40284096 著者名 Teshima, Takanori
言語	英語
キーワード	FIP1L1
	RARA
	PDGFRA
	Leukemia
発行日	2014-09
出版者	Springer
収録物名	Annals of Hematology
巻(号)	93(9)
ページ	1473-1481
抄録	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.
資源タイプ	学術雑誌論文
出版タイプ	Accepted Manuscript
権利情報	The final publication is available at link.springer.com
PISSN	0939-5555
関連情報	PMID 24763514
関連情報 (isVersionOf)	出版社版DOI https://doi.org/10.1007/s00277-014-2085-1