Sato H, Tsukada T, Nagayoshi M, Ikawa Y, Aizawa S, Kato M V
Laboratory of Molecular Oncology, Tsukuba Life Science Center, Ibaraki, Japan.
Biochem Biophys Res Commun. 1995 Sep 14;214(2):468-74. doi: 10.1006/bbrc.1995.2310.
Lambda ZAP cDNA library constructed from spleen of a p53-deficient mouse was screened by South-Western technique using Fragment A, a DNA sequence that p53 specifically binds to, as a probe. One (clone 2) of six clones isolated was identical to MEF2c, a MADS-family transcription factor. Transcripts of the mef2c gene was also detected in spleen where the expression has not been reported so far. Isolated clones except clone 2 had a growth-suppression activity on p53-deficient osteosarcoma cell line (Saos II). Clone 2 repressed the transactivation from Fragment A by p53, suggesting that MEF2c may act as a negative regulator of p53-responsive element.
用p53特异性结合的DNA序列片段A作为探针，通过South-Western技术筛选从小鼠脾脏构建的Lambda ZAP cDNA文库。所分离出的6个克隆中有一个（克隆2）与MEF2c相同，MEF2c是一种MADS家族转录因子。在脾脏中也检测到了mef2c基因的转录本，目前尚未见该基因在脾脏中表达的报道。除克隆2外，所分离出的其他克隆对p53缺陷型骨肉瘤细胞系（Saos II）具有生长抑制活性。克隆2抑制了p53对片段A的反式激活作用，提示MEF2c可能作为p53反应元件的负性调节因子发挥作用。
