SS-A/Ro52 promotes apoptosis by regulating Bcl-2 production

Siti Nur Aisyah Jauharoh, Jun Saegusa, Takeshi Sugimoto, Bambang Ardianto, Shimpei Kasagi, Daisuke Sugiyama, Chiyo Kurimoto, Osamu Tokuno, Yuji Nakamachi, Shunichi Kumagai, Seiji Kawano

研究成果: Article査読

41 被引用数 (Scopus)

抄録

SS-A/Ro52 (Ro52), an autoantigen in systemic autoimmune diseases such as systemic lupus erythematosus and Sjögren's syndrome, has E3 ligase activity to ubiquitinate proteins that protect against viral infection. To investigate Ro52's role during stress, we transiently knocked it down in HeLa cells by siRo52 transfection. We found that Ro52 low HeLa cells were significantly more resistant to apoptosis than wild-type HeLa cells when stimulated by H 2O 2- or diamide-induced oxidative stress, IFN-α, IFN-γ and anti-Fas antibody, etoposide, or γ-irradiation. Furthermore, Ro52-mediated apoptosis was not influenced by p53 protein level in HeLa cells. Depleting Ro52 in HeLa cells caused Bcl-2, but not other Bcl-2 family molecules, to be upregulated. Taken together, our data showed that Ro52 is a universal proapoptotic molecule, and that its proapoptotic effect does not depend on p53, but is exerted through negative regulation of the anti-apoptotic protein Bcl-2. These findings shed light on a new physiological role for Ro52 that is important to intracellular immunity.

本文言語English
ページ(範囲)582-587
ページ数6
ジャーナルBiochemical and Biophysical Research Communications
417
1
DOI
出版ステータスPublished - 2012 1月 6
外部発表はい

ASJC Scopus subject areas

  • 生物理学
  • 生化学
  • 分子生物学
  • 細胞生物学

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