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  1. C. 医薬保健学域; 医学類・薬学類・医薬科学類・保健学類
  2. c 10. 学術雑誌掲載論文(医・保健)
  3. 2.査読済論文(薬)

Signaling pathway for phagocyte priming upon encounter with apoptotic cells

http://hdl.handle.net/2297/48429
http://hdl.handle.net/2297/48429
32f7e238-f605-4ca2-a9b6-2197b9b36e41
名前 / ファイル ライセンス アクション
PH-PR-NONAKA-S-8059.pdf PH-PR-NONAKA-S-8059.pdf (2.3 MB)
Item type 学術雑誌論文 / Journal Article(1)
公開日 2017-12-05
タイトル
タイトル Signaling pathway for phagocyte priming upon encounter with apoptotic 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
著者 Nonaka, Saori

× Nonaka, Saori

WEKO 1186
金沢大学研究者情報 40767787
研究者番号 40767787

Nonaka, Saori

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Ando, Yuki

× Ando, Yuki

WEKO 68979

Ando, Yuki

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Kanetani, Takuto

× Kanetani, Takuto

WEKO 68980

Kanetani, Takuto

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Hoshi, Chiharu

× Hoshi, Chiharu

WEKO 68981

Hoshi, Chiharu

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Nakai, Yuji

× Nakai, Yuji

WEKO 891
金沢大学研究者情報 10321788
研究者番号 10321788

Nakai, Yuji

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Nainu, Firzan

× Nainu, Firzan

WEKO 68982

Nainu, Firzan

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Nagaosa, Kaz

× Nagaosa, Kaz

WEKO 68983

Nagaosa, Kaz

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Shiratsuchi, Akiko

× Shiratsuchi, Akiko

WEKO 27298
金沢大学研究者情報 90303297
研究者番号 90303297

Shiratsuchi, Akiko

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Nakanishi, Yoshinobu

× Nakanishi, Yoshinobu

WEKO 103
e-Rad 40172358
金沢大学研究者情報 40172358
研究者番号 40172358

Nakanishi, Yoshinobu

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書誌情報 Journal of Biological Chemistry

巻 292, 号 19, p. 8059-8072, 発行日 2017-05-12
ISSN
収録物識別子タイプ ISSN
収録物識別子 0021-9258
NCID
収録物識別子タイプ NCID
収録物識別子 AA00251083
DOI
関連タイプ isIdenticalTo
識別子タイプ DOI
関連識別子 10.1074/jbc.M116.769745
出版者
出版者 American Society for Biochemistry and Molecular Biology Inc.
抄録
内容記述タイプ Abstract
内容記述 The phagocytic elimination of cells undergoing apoptosis is an evolutionarily conserved innate immune mechanism for eliminating unnecessary cells. Previous studies showed an increase in the level of engulfment receptors in phagocytes after the phagocytosis of apoptotic cells, which leads to the enhancement of their phagocytic activity. However, precise mechanisms underlying this phenomenon require further clarification. We found that the pre-incubation of a Drosophila phagocyte cell line with the fragments of apoptotic cells enhanced the subsequent phagocytosis of apoptotic cells, accompanied by an augmented expression of the engulfment receptors Draper and integrin αPS3. The DNA-binding activity of the transcription repressor Tailless was transiently raised in those phagocytes, depending on two partially overlapping signal-transduction pathways for the induction of phagocytosis as well as the occurrence of engulfment. The RNAi knockdown of tailless in phagocytes abrogated the enhancement of both phagocytosis and engulfment receptor expression. Furthermore, the hemocytespecific RNAi of tailless reduced apoptotic cell clearance in Drosophila embryos. Taken together, we propose the following mechanism for the activation of Drosophila phagocytes after an encounter with apoptotic cells: two partially overlapping signal-transduction pathways for phagocytosis are initiated; transcription repressor Tailless is activated; expression of engulfment receptors is stimulated; and phagocytic activity is enhanced. This phenomenon most likely ensures the phagocytic elimination of apoptotic cells by stimulated phagocytes and is thus considered as a mechanism to prime phagocytes in innate immunity. © 2017 by The American Society for Biochemistry and Molecular Biology, Inc.
内容記述
内容記述タイプ Other
内容記述 Embargo Period 12 months
著者版フラグ
出版タイプ VoR
出版タイプResource http://purl.org/coar/version/c_970fb48d4fbd8a85
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