p73beta, a variant of p73, enhances Wnt/beta-catenin signaling in Saos-2 cells.

p73beta, a variant of p73, enhances Wnt/beta-catenin signaling in Saos-2 cells.
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p73beta 是 p73 的变体,可增强 Saos-2 细胞中的 Wnt/β-catenin 信号传导。

DOI:
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发表时间:
2001
期刊:
Biochemical and Biophysical Research Communications - BBRC
影响因子:
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通讯作者:
K. Shimotohno
K. Shimotohno
中科院分区:
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文献类型:
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作者:
Y. Ueda;M. Hijikata;S. Takagi;R. Takada;S. Takada;T. Chiba;K. Shimotohno

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Wnt/β-catenin通路和P53是结直肠癌基因改变的常见靶点,它们之间的关系已有报道。在这里,我们描述了Wnt/β-catenin信号与P53相关基因p73的关系。在Saos-2细胞中,P73激活的是含有Tcf结合序列的启动子,而不是P53,且激活程度与P53反应的启动子的激活程度呈正相关。此外,与P53不同的是,p73β与WNT-3a协同增强Wnt/β-catenin信号转导或外源表达β-catenin,且这种增强不是由β-catenin积聚引起的。这些结果表明,p73在Wnt/β-catenin信号转导中的作用与p53不同。
The Wnt/beta-catenin pathway and p53 are very common targets for genetic alterations in colorectal cancer, and relationships between them have been reported. Here, we describe the relation between Wnt/beta-catenin signaling and the p53-related gene p73. p73, but not p53, activated a promoter containing the Tcf-binding sequence in Saos-2 cells, and the degree of activation was positively correlated with that on a p53-responsive promoter. Moreover, p73beta enhanced Wnt/beta-catenin signaling synergistically with Wnt-3a or exogenously expressed beta-catenin, unlike p53, and the enhancement was not caused by the accumulation of beta-catenin. These results show that the effects of p73 on Wnt/beta-catenin signaling differ from those of p53.