J
Ji-Hyeon Lee
Researcher at National Institutes of Health
Publications - 12
Citations - 1009
Ji-Hyeon Lee is an academic researcher from National Institutes of Health. The author has contributed to research in topics: Pancreas & Signal transduction. The author has an hindex of 8, co-authored 11 publications receiving 777 citations.
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Journal ArticleDOI
Beneficial Metabolic Effects of a Probiotic via Butyrate-induced GLP-1 Hormone Secretion
TL;DR: It is demonstrated that the administration of a probiotic, VSL#3, prevented and treated obesity and diabetes in several mouse models and suggested that probiotics can modulate the gut microbiota-SCFA-hormone axis.
Journal ArticleDOI
Transforming Growth Factor-β/Smad3 Signaling Regulates Insulin Gene Transcription and Pancreatic Islet β-Cell Function
Huei-Min Lin,Ji-Hyeon Lee,Hariom Yadav,Anil K. Kamaraju,Eric Liu,Duan Zhigang,Anthony Vieira,Seong-Jin Kim,Heather W. Collins,Franz M. Matschinsky,David M. Harlan,Anita B. Roberts,Sushil G. Rane +12 more
TL;DR: These studies emphasize TGF-β/Smad3 signaling as an important regulator of insulin gene transcription and β-cell function and suggest that components of the T GF-β signaling pathway may be dysregulated in diabetes.
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Transforming growth factor-β pathway: Role in pancreas development and pancreatic disease
TL;DR: Although TGF-beta still remains elusive in terms of the authors' understanding of its multifunctional modes of action, research is moving closer to the design of approaches directed toward modulating its activities for therapeutic benefit.
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Tumor formation via loss of a molecular motor protein.
TL;DR: The results support the notion that loss of a molecular motor leads to tumor formation and that aneuploidy can act as a primary trigger of tumorigenesis.
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Transformation resistance in a premature aging disorder identifies a tumor-protective function of BRD4.
TL;DR: It is found that HGPS cells are resistant to neoplastic transformation, mediated by the bromodomain protein BRD4, which exhibits altered genome-wide binding patterns in transformation-resistant cells, leading to inhibition of oncogenic dedifferentiation.