p53 is a mediator for radiation-repressed human TR2 orphan receptor expression in MCF-7 cells, a new pathway from tumor suppressor to member of the steroid receptor superfamily

p53 is a mediator for radiation-repressed human TR2 orphan receptor expression in MCF-7 cells, a new pathway from tumor suppressor to member of the steroid receptor superfamily
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DOI:
10.1074/jbc.271.25.14649
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发表时间:
1996-06-21
影响因子:
4.8
通讯作者:
Chang, CS
Chang, CS
中科院分区:
生物学2区
文献类型:
--
作者:
Lin, DL;Chang, CS

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P53可能作为一个检查点,在辐射或其他刺激引起的DNA损伤反应中阻止G(1)细胞周期。我们发现,作为类固醇受体超家族的一员,TR2孤儿受体(TR2)的表达受到电离辐射的下调。我们的研究结果表明,辐射可以在翻译和转录水平上抑制TR2。瞬时转染实验进一步将p53与这种抑制联系在一起,证明了内源性或外源性的P53可以抑制TR2基因的表达,并且这种抑制可以被SV40大T抗原的共转染所逆转。综上所述,我们的数据首次证明了辐射和P53可以抑制TR2,这可能提供了一条将电离辐射和P53与类固醇受体超家族成员联系起来的新途径。
p53 may function as a checkpoint by arresting the G(1) cell cycle in response to DNA damage induced by radiation or other stimuli. We have found that the expression of the TR2 orphan receptor (TR2), a member of the steroid receptor superfamily, was down-regulated by ionizing irradiation, Our data shown in the present study demonstrate that irradiation can repress TR2 at both the translational and transcriptional levels. Transient transfection assays further link p53 to this repression by proving that endogenously induced or exogenously transfected p53 can repress TR2 gene expression, and this repression can be reversed by the co-transfection of SV40 large T antigen. Together, our data demonstrate for the first time that radiation and p53 can repress TR2, possibly providing a new pathway to link ionizing irradiation and p53 to members of the steroid receptor superfamily.