Selenium chitosan by promoting PML RARα fusion protein and molecular chaperone Hsp90 fusion protein reduced the level of dissociation_0.docVIP
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Selenium chitosan by promoting PML RARα fusion protein and molecular chaperone Hsp90 fusion protein reduced the level of dissociation
Of: Deng Shouheng, Cai Xiaojun, Li Lin Jun, Yuyuan Dong, Li Fang, Chen Ping
[Abstract] Objective To study the selenium chitosan (Sc) NB4 cells reduced the fusion protein PML RAR @ role and relationship between the molecular chaperone Hsp90. Method by flow cytometry and Western blotting Sc treated NB4 cells PML RAR @ Fusion protein, Hsp90 content changes; RT PCR analysis Sc treated cells PML RAR @ mRNA level changes. The results can be reduced Sc NB4 cells PML RAR @ fusion protein, showed dose-effect relationship, 50,100,200 mg / L Sc for 24 h, cells PML RAR @ fusion protein positive rate was 62.8%, 33.14%, 17.07%, Sc on the cell PML RAR @ mRNA levels were not affected; 50,100,200 mg / L Sc NB4 cells 24 h treatment of intracellular Hsp90 levels could reduced. Conclusions down PML RAR @ Sc fusion protein content, primarily through inhibition of Hsp90 chaperone function, so that PML RAR @ fusion protein and Hsp90 protein dissociation, PML RAR @ loss of normal stability of the fusion protein and then degraded.
[Keywords:] Selenium Chitosan; PML RAR @ fusion protein; Hsp90
Chitosan is present in the biological nature of a basic polysaccharide, because of its excellent biocompatibility, almost no toxicity, no other adverse reactions, drug preparation in the modern drugs are often used as a good material for development. Selenide shell glycans [1] (Selenium chitosan, Sc) is a low molecular weight chitosan and selenite in acid conditions, the mixed metal ions as the catalyst, prepared from the principle by merging an organic selenium. The preliminary study group The results showed that Sc could inhibit the proliferation of human acute promyelocytic leukemia NB4 cells, some PML RAR @ Bennett fusion protein and the Ras-mediated signaling and other ways to inhibit cell proliferation, induce apoptosis [2].
Heat shock protein (heat
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