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KMID : 0624620160490060325
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BMB Reports
2016 Volume.49 No. 6 p.325 ~ p.330
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TCP10L synergizes with MAD1 in transcriptional suppression and cell cycle arrest through mutual interaction
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Shen Suqin
Zuo Jie
Feng Huan
Bai Meirong
Wang Chenji
Wei Youheng
Li Yanhong
Le Yichen
Wu Jiaxue
Wu Yanhua
Wu Yanhua
Yu Long
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Abstract
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T-complex protein 10A homolog 2 (TCP10L) was previously demonstrated to be a potential tumor suppressor in human hepatocellular carcinoma (HCC). However, little is known about the molecular mechanism. MAX dimerization protein 1 (MAD1) is a key transcription suppressor that is involved in regulating cell cycle progression and Myc-mediated cell transformation. In this study, we identified MAD1 as a novel TCP10L-interacting protein. The interaction depends on the leucine zipper domain of both TCP10L and MAD1. TCP10L, but not the interaction-deficient TCP10L mutant, synergizes with MAD1 in transcriptional repression, cell cycle G1 arrest and cell growth suppression. Mechanistic exploration further revealed that TCP10L is able to stabilize intracellular MAD1 protein level. Consistently, the MAD1-interaction-deficient TCP10L mutant exerts no effect on stabilizing the MAD1 protein. Taken together, our results strongly indicate that TCP10L stabilizes MAD1 protein level through direct interaction, and they cooperatively regulate cell cycle progression.
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KEYWORD
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Hepatocellular carcinoma, MAX dimerization protein 1, Protein degradation, Protein-protein interaction, T-complex protein 10A homolog 2
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