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  1. 原著論文

Enhanced expression of the early retrotransposon in C3H mouse-derived myeloid leukemia cells

https://repo.qst.go.jp/records/42918
https://repo.qst.go.jp/records/42918
bc4d8c90-64e8-43a6-93cd-9a6f77004c5c
Item type 学術雑誌論文 / Journal Article(1)
公開日 2002-06-10
タイトル
タイトル Enhanced expression of the early retrotransposon in C3H mouse-derived myeloid leukemia cells
言語
言語 eng
資源タイプ
資源タイプ識別子 http://purl.org/coar/resource_type/c_6501
資源タイプ journal article
アクセス権
アクセス権 metadata only access
アクセス権URI http://purl.org/coar/access_right/c_14cb
著者 Tanaka, Izumi

× Tanaka, Izumi

WEKO 427110

Tanaka, Izumi

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Ishihara, Hiroshi

× Ishihara, Hiroshi

WEKO 427111

Ishihara, Hiroshi

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田中 泉

× 田中 泉

WEKO 427112

en 田中 泉

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石原 弘

× 石原 弘

WEKO 427113

en 石原 弘

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内容記述タイプ Abstract
内容記述 Cells of acute myeloid leukemia (AML) from C3H/He mice express an increased amount of RNA for an endogenous retrovirus-like retrotransposon, intracisternal A-particle element. We analyzed the transcription of other mouse retrotransposons in C3H-derived tumor cells and found that all the AML lines from different mice overexpress early-transposon (ETn) RNA. In contrast, only faint levels of ETn were detected in the cells from other tumors, including hepatoma and lymphoma. The polyadenylation sites of the ETn RNA in the AML cells varied. We also determined the binding site for the nuclear extract of the AML cells in the long terminal repeat sequence of ETn. The overexpression of ETn as a common phenotype of AML cells suggests that myeloid cells with this phenotype are the origin of all the AML cells or that the phenotype is acquired during leukemogenesis.
書誌情報 Virology

巻 280, p. 107-114, 発行日 2001-01
ISSN
収録物識別子タイプ ISSN
収録物識別子 0042-6822
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