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  1. 医学科
  2. 内科学講座 消化器・血液
  3. 学術雑誌掲載論文等(内科学講座 消化器・血液)

LSD1-mediated repression of GFI1 super-enhancer plays an essential role in erythroleukemia.

http://hdl.handle.net/10422/00012579
http://hdl.handle.net/10422/00012579
581ddc00-2ae3-4a81-89c6-08559c394187
名前 / ファイル ライセンス アクション
s41375-019-0614-6.pdf s41375-019-0614-6 (7.2 MB)
© The Author(s), under exclusive licence to Springer Nature Limited 2019
Supplementary Supplementary information_s41375-019-0614-6 (1.8 MB)
© The Author(s), under exclusive licence to Springer Nature Limited 2019
Item type 学術雑誌論文 / Journal Article(1)
公開日 2019-11-25
タイトル
タイトル LSD1-mediated repression of GFI1 super-enhancer plays an essential role in erythroleukemia.
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
著者 TATSUMI, Goichi

× TATSUMI, Goichi

WEKO 7633
ORCID 0000-0001-5886-2381

TATSUMI, Goichi

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KAWAHARA, Masahiro

× KAWAHARA, Masahiro

WEKO 7509
e-Rad 80617449
ORCID 0000-0002-2721-7571

KAWAHARA, Masahiro

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YAMAMOTO, Ryusuke

× YAMAMOTO, Ryusuke

WEKO 7634

YAMAMOTO, Ryusuke

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HISHIZAWA, Masakatsu

× HISHIZAWA, Masakatsu

WEKO 7635

HISHIZAWA, Masakatsu

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KITO, Katsuyuki

× KITO, Katsuyuki

WEKO 314

KITO, Katsuyuki

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SUZUKI, Takayoshi

× SUZUKI, Takayoshi

WEKO 7636

SUZUKI, Takayoshi

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TAKAORI-KONDO, Akifumi

× TAKAORI-KONDO, Akifumi

WEKO 7637

TAKAORI-KONDO, Akifumi

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ANDOH, Akira

× ANDOH, Akira

WEKO 644
e-Rad 90252395
ORCID 0000-0001-8533-2669

ANDOH, Akira

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著者別名 辰巳, 剛一

× 辰巳, 剛一

WEKO 7633
ORCID 0000-0001-5886-2381

辰巳, 剛一

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河原, 真大

× 河原, 真大

WEKO 7509
e-Rad 80617449
ORCID 0000-0002-2721-7571

河原, 真大

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木藤, 克之

× 木藤, 克之

WEKO 314

木藤, 克之

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安藤, 朗

× 安藤, 朗

WEKO 644
e-Rad 90252395
ORCID 0000-0001-8533-2669

安藤, 朗

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抄録
内容記述タイプ Abstract
内容記述 Super-enhancers (SEs) consist of enhancer clusters with abundant binding of transcription factors (TFs) and cofactors. LSD1 is a histone modifier that eliminates SE activity. However, whether SE suppression by LSD1 is associated with leukemogenesis remains unknown. In erythro-megakaryocyte lineage leukemia cells, activation of the SE of GFI1 (GFI1-SE) is related to induction of myeloid differentiation by LSD1 inhibitors NCD38 and NCD25 and to their antileukemia effect. Although functional TF-motifs were concentrated in an evolutionally conserved area, NCD38 barely induced additional TF recruitment. Instead, the transcription cofactors including LSD1, CoREST, HDAC1, and HDAC2 were evicted from GFI1-SE. Deletion of GFI1-SE impaired induction of myeloid differentiation by NCD38 and NCD25 in erythroleukemia cells. Gene set enrichment analysis revealed that the GFI1-SE deletion impaired NCD38-induced programs related to granulocyte differentiation and the CEBPA network, but restored NCD38-suppressed programs related to erythroid development, GATA1 targets, and acute myeloid leukemia (AML) clusters including FAB subtype M6 and AML with myelodysplastic syndrome-related chromosomal abnormalities. Ontologies of genes whose expression changes by NCD38 were canceled due to the GFI1-SE deletion showed enrichment in AML and neutropenia signatures. Collectively, our data suggest that sustainable repression of GFI1-SE by LSD1 is essential for sustenance of erythroleukemia cells.
書誌情報 en : Leukemia

発行日 2019-11-01
出版者
出版者 Nature Publishing Group
ISSN
収録物識別子タイプ ISSN
収録物識別子 1476-5551
PMID
関連タイプ isVersionOf
識別子タイプ PMID
関連識別子 31676828
DOI
関連タイプ isVersionOf
識別子タイプ DOI
関連識別子 https://doi.org/10.1038/s41375-019-0614-6
関連名称 10.1038/s41375-019-0614-6
権利
権利情報 © The Author(s), under exclusive licence to Springer Nature Limited 2019
著者版フラグ
出版タイプ AM
出版タイプResource http://purl.org/coar/version/c_ab4af688f83e57aa
資源タイプ
内容記述タイプ Other
内容記述 Journal Article
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