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Human Liver Specific Transcriptional Factor TCP10L Binds to MAD4
Jiang, Dao-Jun,Yu, Hong-Xiu,Hexige, Sa-Yin,Guo, Ze-Kun,Wang, Xiang,Ma, Li-Jie,Chen, Zheng,Zhao, Shou-Yuan,Yu, Long Korean Society for Biochemistry and Molecular Biol 2004 Journal of biochemistry and molecular biology Vol.37 No.4
A human gene T-complex protein 10 like (TCP10L) was cloned in our lab. A previous study showed that it expressed specifically in the liver and testis. A transcription experiment revealed that TCP10L was a transcription factor with transcription inhibition activity. In this study, the human MAD4 was identified to interact with TCP10L by a yeast two-hybrid screen. This finding was confirmed by immunoprecipitation and subcellular localization experiments. As MAD4 is a member of the MAD family, which antagonizes the functions of MYC and promotes cell differentiation, the biological function of the interaction between TCP10L and MAD4 may be to maintain the differentiation state in liver cells. Also, we propose that the up-regulation of Myc is caused by the down-regulation of TCP10L in human hepatocarcinomas.
Human Liver Specific Transcriptional Factor TCP10L Binds to MAD4
( Dao Jun Jiang ),( Hong Xiu Yu ),( Sa Yin Hexige ),( Ze Kun Guo ),( Xiang Wang ),( Li Jie Ma ),( Zheng Chen ),( Shou Yuan Zhao ),( Long Yu ) 생화학분자생물학회 2004 BMB Reports Vol.37 No.4
A human gene T-complex protein 10 like (TCP10L) was cloned in our lab. A previous study showed that it expressed specifically in the liver and testis. A transcription experiment revealed that TCP10L was a transcription factor with transcription inhibition activity. In this study, the human MAD4 was identified to interact with TCP10L by a yeast two-hybrid screen. This finding was confirmed by immunoprecipitation and subcellular localization experiments. As MAD4 is a member of the MAD family, which antagonizes the functions of MYC and promotes cell differentiation, the biological function of the interaction between TCP10L and MAD4 may be to maintain the differentiation state in liver cells. Also, we propose that the up-regulation of Myc is caused by the down-regulation of TCPIOL in human hepatocarcinomas.