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タイトル
  • en Involvement of STAP-2 in Brk-mediated phosphorylation and activation of STAT5 in breast cancer cells.
作成者
アクセス権 open access
権利情報
  • en The definitive version is available at www.blackwell-synergy.com
主題
  • Other en Brk
  • Other en STAP-2
  • Other en STAT5
  • Other en phosphorylation
  • Other en breast cancer
  • NDC 499
内容注記
  • Abstract en Signal-transducing adaptor protein (STAP)-2 is a recently identified adaptor protein that contains Pleckstrin homology (PH) and Src homology 2 (SH2)-like domains, and is also known to be a substrate of breast tumor kinase (Brk). In a previous study, we found that STAP-2 upregulated Brk-mediated activation of signal transducer and activator of transcription (STAT) 3 in breast cancer cells. Here, we examined the involvement of STAP-2 in Brk-mediated STAT5 activation in breast cancer cells. Ectopic expression of STAP-2 induced Brk-mediated transcriptional activity of STAT5. Furthermore, STAP-2-knockdown in T47D breast cancer cells induced a marked decrease in proliferation that was as strong as that after Brk- or STAT5b-knockdown. Regarding the mechanism, the PH domain of STAP-2 is likely to participate in the process by which Brk phosphorylates and activates STAT5. Taken together, our findings provide insights toward the development of novel therapeutic strategies as well as novel prognostic values in breast carcinomas.
出版者 en Wiley
日付
    Issued2011-04
言語
  • eng
資源タイプ journal article
出版タイプ AM
資源識別子 HDL http://hdl.handle.net/2115/48965
関連
  • isVersionOf DOI https://doi.org/10.1111/j.1349-7006.2010.01842.x
  • PMID 21205088
収録誌情報
    • PISSN 1347-9032
    • EISSN 1349-7006
    • NCID AA11808050
      • en Cancer Science
      • 102 4 開始ページ756 終了ページ761
ファイル
コンテンツ更新日時 2023-10-07