Qiwei Zhai

Shanghai Institutes for Biological Sciences, Shanghai, Shanghai Shi, China

Are you Qiwei Zhai?

Claim your profile

Publications (5)13.45 Total impact

  • [Show abstract] [Hide abstract]
    ABSTRACT: A tet-off inducible cell line named BBT derived from BA/F3β cell line was constructed and the effect of this inducible expression system was significant when detected by tet-off responded luciferase reporter gene assay. Then tet-off responded Akt expression plasmid was transfected into BBT cells, and the stable cell lines were screened. The result of Northern blot showed that the expression ofakt was significantly inducible. The clone with the best inducible effect was selected and named BBA for investigating the function of Akt. We found that Akt could significantly inhibit zinc-induced decrease of cell viability when assayed by MTT method. And the flow cytometric analysis showed that Akt could markedly repress zinc-induced apoptosis. Keywordsinducible expression system-Akt-apoptosis
    Chinese Science Bulletin 01/2001; 46(3):222-225. · 1.37 Impact Factor
  • Q Zhai, H Ji, Z Zheng, X Yu, L Sun, X Liu
    [Show abstract] [Hide abstract]
    ABSTRACT: Copper, an essential trace element, can be toxic to some cells when present in excess. But thorough investigations into the cytotoxicity of copper and subsequent molecular mechanisms are rare, although the cytotoxicity of copper has been applied to cancer chemotherapy. The present study demonstrates that Cu(2+) inhibits [(3)H] thymidine incorporation in mouse pro-B cell line BA/F3beta and induces apoptosis. Apoptosis was mainly judged by morphology of cells, quantification of subdiploid DNA contents by flow cytometry, and detection of DNA fragmentation by gel electrophoresis. The apoptotic effect is dose and time dependent. Western blotting shows Bax is upregulated by Cu(2+). Bcl-2 overexpression can partially inhibit this apoptosis. Moreover, Cu(2+) increases the production of reactive oxygen species (ROS) in a dose-dependent manner. The antioxidant N-acetylcysteine (NAC) not only significantly inhibited copper-induced apoptosis but also totally blocked generation of ROS, while Bcl-2 overexpression has no effect on the generation of ROS. Furthermore, our results show that NFkappaB is downregulated by Cu(2+). Bcl-2 overexpression or NAC can sustain the activity of NFkappaB. These data indicate that Cu(2+) might induce apoptosis in BA/F3beta cells via upregulation of Bax and ROS and subsequent inactivation of NFkappaB.
    Journal of Cellular Physiology 09/2000; 184(2):161-70. · 4.22 Impact Factor
  • [Show abstract] [Hide abstract]
    ABSTRACT: Copper, an essential trace element, can be toxic to some cells when present in excess. But thorough investigations into the cytotoxicity of copper and subsequent molecular mechanisms are rare, although the cytotoxicity of copper has been applied to cancer chemotherapy. The present study demonstrates that Cu2+ inhibits [3H] thymidine incorporation in mouse pro-B cell line BA/F3β and induces apoptosis. Apoptosis was mainly judged by morphology of cells, quantification of subdiploid DNA contents by flow cytometry, and detection of DNA fragmentation by gel electrophoresis. The apoptotic effect is dose and time dependent. Western blotting shows Bax is upregulated by Cu2+. Bcl-2 overexpression can partially inhibit this apoptosis. Moreover, Cu2+ increases the production of reactive oxygen species (ROS) in a dose-dependent manner. The antioxidant N-acetylcysteine (NAC) not only significantly inhibited copper-induced apoptosis but also totally blocked generation of ROS, while Bcl-2 overexpression has no effect on the generation of ROS. Furthermore, our results show that NFκB is downregulated by Cu2+. Bcl-2 overexpression or NAC can sustain the activity of NFκB. These data indicate that Cu2+ might induce apoptosis in BA/F3β cells via upregulation of Bax and ROS and subsequent inactivation of NFκB. J. Cell. Physiol. 184:161–170, 2000. © 2000 Wiley-Liss, Inc.
    Journal of Cellular Physiology 06/2000; 184(2):161 - 170. · 4.22 Impact Factor
  • [Show abstract] [Hide abstract]
    ABSTRACT: To find a possible signal interacting with the Jak3 N-terminal, we screened the human peripheral blood cDNA library through both a two-hybrid system and a tyrosine-phosphorylation-modified two-hybrid system using the N-terminal of Jak3 as bait. Results showed that one new homologue of myosin heavy chain, designated MAJN (molecule associated with Jak3 N-terminal), could bind to Jak3 in a tyrosine-phosphorylation-independent manner. The interaction between Jak3 and MAJN was further confirmed by immunoprecipitation in BAF-B03 beta cells. To investigate the function of MAJN, we have constructed the BAF-B03 beta/MAJN cell line that stably expresses MAJN and found that overexpression of MAJN can partially inhibit the apoptosis induced by interleukin-2 deprival. Further studies are needed to elucidate how MAJN executes its function to antagonize BAF-B03beta cell death in the absence of IL-2.
    Biochemical and Biophysical Research Communications 05/2000; 270(1):267-71. · 2.28 Impact Factor
  • [Show abstract] [Hide abstract]
    ABSTRACT: Interferonα (IFNα) and interleukin-2 (IL-2) are crucial cytokines in immune system. They also play an important role in nerve system. It has been reported that IL-2 can induce the central analgesia. It is demonstrated that IFNα also can induce the peripheral analgesia, which can be blocked by naloxone as IL-2. Furthermore, the analgesic effect of IFN-α is reversible by monoclonal anti-IL-2 antibody.In vitro experiments show that IFN-α significantly increases the production of IL-2 in a dose dependent manner. These data suggest that IL-2 mediates the peripheral analgesia of IFN-α.
    Chinese Science Bulletin 01/1999; 44(3):243-246. · 1.37 Impact Factor

Publication Stats

61 Citations
13.45 Total Impact Points

Institutions

  • 2001
    • Shanghai Institutes for Biological Sciences
      Shanghai, Shanghai Shi, China
  • 2000
    • Chinese Academy of Sciences
      Peping, Beijing, China