Jin Yu
Yale University
5 Papers
157 Citations
Jin Yu is an academic researcher from Yale University. The author has contributed to research in topics: Transcription factor & Transactivation. The author has an hindex of 5, co-authored 5 publications.
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Papers
The interferon-inducible p204 protein acts as a transcriptional coactivator of Cbfa1 and enhances osteoblast differentiation.
Chuan-ju Liu,Eric Y. Chang,Jin Yu,Cathy S. Carlson,Lisa Prazak,Xiu Ping Yu,Bo Ding,Peter Lengyel,Paul E. Di Cesare +8 more
TL;DR: In this article, an interferon-inducible protein, p204, was shown to inhibit cell proliferation and promote the differentiation of myoblasts to myotubes, is a novel regulator in the course of osteogenesis.
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The Retinoblastoma Protein Is an Essential Mediator of Osteogenesis That Links the p204 Protein to the Cbfa1 Transcription Factor Thereby Increasing Its Activity
Yi Luan,Yi Luan,Xiuping Yu,Ke Xu,Bo Ding,Jin Yu,Yan Huang,Ning Yang,Peter Lengyel,Paul E. Di Cesare,Chuan-ju Liu,Chuan-ju Liu +11 more
TL;DR: It is established that suppression of p204 expression by an adenovirus construct encoding p204 antisense RNA inhibited osteoblast-specific gene activation by Cbfa1 in an osteogenesis assay involving the pluripotent C2C12 mesenchymal cell line.
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p204 Protein Overcomes the Inhibition of the Differentiation of P19 Murine Embryonal Carcinoma Cells to Beating Cardiac Myocytes by Id Proteins
TL;DR: It is reported that endogenous or ectopic inhibitor of differentiation (Id) proteins inhibited the differentiation of P19 cells to myocytes, and p204 overcame this inhibition by Id proteins in consequence of binding and sequestering Id proteins, and accelerating their ubiquitination and degradation by proteasomes.
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p204 Is Required for the Differentiation of P19 Murine Embryonal Carcinoma Cells to Beating Cardiac Myocytes ITS EXPRESSION IS ACTIVATED BY THE CARDIAC GATA4, NKX2.5, AND TBX5 PROTEINS
TL;DR: It is reported that the MyoD-inducible p204 protein was also required for the differentiation of cultured P19 murine embryonal carcinoma stem cells to beating cardiac myocytes and was synergistically transactivated by the cardiac Gata4, Nkx2.5, and Tbx5 transcription factors.
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IFI16 inhibits tumorigenicity and cell proliferation of bone and cartilage tumor cells.
TL;DR: Overexpression of functional IFI16 in human osteosarcomas and chondrosarcoma cell lines markedly inhibited colony formation, and significantly inhibited cell growth, an effect that could be reversed by introduction of gene specific siRNA into tumor cells.
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