共查询到20条相似文献,搜索用时 46 毫秒
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The Mad and Myc basic domains are functionally equivalent 总被引:4,自引:0,他引:4
Nikiforov MA Popov N Kotenko I Henriksson M Cole MD 《The Journal of biological chemistry》2003,278(13):11094-11099
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P J Hurlin C Quéva P J Koskinen E Steingrímsson D E Ayer N G Copeland N A Jenkins R N Eisenman 《The EMBO journal》1995,14(22):5646-5659
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mad—overexpression down regulates the malignant growth and p53 mediated apoptosis in human hepatocellular carcinoma BEL—7404 cells 总被引:4,自引:0,他引:4
ZHANHUA YONGHUAXU 《Cell research》1999,9(1):51-59
Mad protein has been shown as an antagonist of cMyc protein in some cell lines.The effect of Mad protein to the malignant phenotype of human hepatoma BEL-7404 cell line was investigated experimentally.An eukarryotic vector pCDNA Ⅲ containing full ORF fragment of mad cDNA was transfected into targeted cells.Under G418 selection,stable Mad-overexpressed cells were cloned.Studies on the effect of Mad over-expression in cell proliferation and cell cycle revealed that cell morphology of the Mad-overexpressed BEL-7404-M1 cells was significantly different from the parent and control vector transfected cells.DNA synthesis,cell proliferation and anchorage-independent growth in soft-agar of the madtransfected cells were partially inhibited in comparison to control cells.Flos cytometry analysis indicated that mad over-expression might block more transfectant cells at G0/G1 phase,resulting in the retardation of cell proliferation.RT-PCR detected a marked inhibition of the expression of cdc25A,an important regulator gene of G0/G1 to S phase in cell cycle.It was also found that Mad protein overexpression could greatly suppress p53-mediated apoptosis in BEL-74040M1 cells in the absence of serume.Thus,Mad proteins may function as a negative regulator antagonizing c-Myc activity in the control of cell growth and apoptosis in human hepatocellular carcinoma BEL-7404 cells. 相似文献
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Hasegawa A Yasukawa M Sakai I Fujita S 《Journal of immunology (Baltimore, Md. : 1950)》2001,166(2):1125-1131
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Function of the c-Myc antagonist Mad1 during a molecular switch from proliferation to differentiation. 总被引:3,自引:1,他引:2
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Mad-Max heterodimers have been shown to antagonize Myc transforming activity by a mechanism requiring multiple protein-protein and protein-DNA interactions. However, the mechanism by which Mad functions in differentiation is unknown. Here, we present evidence that Mad functions by an active repression mechanism to antagonize the growth-promoting function(s) of Myc and bring about a transition from cellular proliferation to differentiation. We demonstrate that exogenously expressed c-Myc blocks inducer-mediated differentiation of murine erythroleukemia cells without disrupting the induction of endogenous Mad; rather, high levels of c-Myc prevent a heterocomplex switch from growth-promoting Myc-Max to growth-inhibitory Mad-Max. Cotransfection of a constitutive c-myc with a zinc-inducible mad1 results in clones expressing both genes, whereby a switch from proliferation to differentiation can be modulated. Whereas cells grown in N'N'-hexamethylene bisacetamide in the absence of zinc fail to differentiate, addition of zinc up-regulates Mad expression by severalfold and differentiation proceeds normally. Coimmunoprecipitation analysis reveals that Mad-Max complexes are in excess of Myc-Max in these cotransfectants. Moreover, we show that the Sin-binding, basic region, and leucine zipper motifs are required for Mad to function during a molecular switch from proliferation to differentiation. 相似文献
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Function of the c-Myc oncogenic transcription factor 总被引:29,自引:0,他引:29
Dang CV Resar LM Emison E Kim S Li Q Prescott JE Wonsey D Zeller K 《Experimental cell research》1999,253(1):63-77
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CIP2A inhibits PP2A in human malignancies 总被引:6,自引:0,他引:6
Junttila MR Puustinen P Niemelä M Ahola R Arnold H Böttzauw T Ala-aho R Nielsen C Ivaska J Taya Y Lu SL Lin S Chan EK Wang XJ Grènman R Kast J Kallunki T Sears R Kähäri VM Westermarck J 《Cell》2007,130(1):51-62
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