[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
[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.
Article · May 2000 · Biochemical and Biophysical Research Communications
[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.