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  1. 川崎医学会機関誌
  2. Kawasaki Medical Journal
  3. Vol.41(2015)
  4. No.2

TNF receptor type 2 transmits caspase-dependent apoptotic signals in fibroblast-like synoviocytes derived from rheumatoid arthritis

https://kwmed.repo.nii.ac.jp/records/580
https://kwmed.repo.nii.ac.jp/records/580
a6eb4089-1b61-4aa7-b2f0-61dad276603e
名前 / ファイル ライセンス アクション
KJ00010041779.pdf KJ00010041779.pdf (1.5 MB)
Item type [ELS]学術雑誌論文 / Journal Article(1)
公開日 2017-01-23
タイトル
タイトル TNF receptor type 2 transmits caspase-dependent apoptotic signals in fibroblast-like synoviocytes derived from rheumatoid arthritis
言語 en
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 Hirano, Hiroyasu

× Hirano, Hiroyasu

en Hirano, Hiroyasu

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Igarashi, Hideya

× Igarashi, Hideya

en Igarashi, Hideya

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Morita, Yoshitaka

× Morita, Yoshitaka

en Morita, Yoshitaka

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Ishihara, Katsuhiko

× Ishihara, Katsuhiko

en Ishihara, Katsuhiko

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著者所属(英)
en
Department of Immunology and Molecular Genetics Kawasaki Medical School
著者所属(英)
en
Department of Immunology and Molecular Genetics Kawasaki Medical School
著者所属(英)
en
Department of Rheumatology Kawasaki Medical School
著者所属(英)
en
Department of Immunology and Molecular Genetics Kawasaki Medical School
キーワード
言語 en
主題Scheme Other
主題 Rheumatoid arthritis
キーワード
言語 en
主題Scheme Other
主題 Fibroblast-like synoviocyte
キーワード
言語 en
主題Scheme Other
主題 Apoptosis
キーワード
言語 en
主題Scheme Other
主題 Caspase
記事種別(英)
内容記述タイプ Other
内容記述 Original Article
言語 en
抄録(英)
en
Signals from tumor necrosis factor α (TNFα) are transduced through two types of receptors, tumor necrosis factor receptor type1 (TNFR1) and type2 (TNFR2), which commonly transduce activation signals for NF-κB, affecting cellular survival, growth, and inflammation. TNFR1 is ubiquitously expressed and mediates caspase-dependent apoptotic signals, whereas TNFR2 is selectively expressed on hematopoietic cells without transducing death signals. We detected TNFR2 transcription in fibroblast-like synoviocytes derived from rheumatoid arthritis (RA-FLS) at various levels, but usually much lower than those of TNFR1. To investigate the function of TNFR2 on RA-FLS in TNFα signaling, we established a stable transfectant overexpressing TNFR2 using the human RA-FLS cell line MH7A and stimulated it with 50ng/ml TNFα, a concentration that usually induces apoptosis in parent MH7A cells. Since TNFR2 is known to transduce anti-apoptotic signals via NF-κB activation, we expected to observe a reduction in apoptotic cells. Contrary to our expectations, the ratio of apoptotic cells in TNFR2 transfectants was higher than that of mock stable transfectants used as a control. This enhanced sensitivity to apoptosis was not inhibited by the addition of either anti-TNFR2 monoclonal antibody (mAb) 80M2, which blocks ligand passing, or antagonistic anti-TNFR1 Ab, indicating that apoptosis was independent of TNFR1 signals. Furthermore, in the presence of antagonistic anti-TNFR1 Ab, the addition of agonistic anti-TNFR2 Ab induced apoptosis with a rapid decrease in TNF receptor-associated factor 2 (TRAF2) and cleavage of caspase-8and-3. The observed apoptosis was sensitive to an inhibitor of pan-caspase, but not of receptor-interacting protein (RIP) 1. These data clearly indicate the presence of a caspasedependent, apoptotic signaling pathway downstream of TNFR2.
書誌情報 en : Kawasaki medical journal

巻 41, 号 2, p. 29-40, 発行日 2015
URL
識別子 http://igakkai.kms-igakkai.com/wp/wp-content/uploads/2015en/KMJ-E41(2)29.pdf
識別子タイプ URI
DOI
識別子タイプ DOI
関連識別子 https://doi.org/10.11482/KMJ-E41(2)29
ISSN
収録物識別子タイプ PISSN
収録物識別子 0385-0234
ISSN
収録物識別子タイプ EISSN
収録物識別子 2434-3404
雑誌書誌ID
収録物識別子タイプ NCID
収録物識別子 AA12685295
雑誌書誌ID
収録物識別子タイプ NCID
収録物識別子 AA12029005
著者版フラグ
出版タイプ VoR
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