H
Huei-Min Lin
Researcher at National Institutes of Health
Publications - 8
Citations - 407
Huei-Min Lin is an academic researcher from National Institutes of Health. The author has contributed to research in topics: Cyclin-dependent kinase & Cyclin D1. The author has an hindex of 6, co-authored 8 publications receiving 378 citations.
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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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Nucleocytoplasmic Shuttling of the Retinoblastoma Tumor Suppressor Protein via Cdk Phosphorylation-dependent Nuclear Export
TL;DR: In this paper, the authors illustrate a function for Cdks in regulating the subcellular localization of retinoblastoma (RB) tumor suppressor protein and uncover a novel mechanism to circumvent RB-mediated growth suppression by altered nucleocytoplasmic trafficking via the Exportin1 pathway.
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Aberrant nucleocytoplasmic localization of the retinoblastoma tumor suppressor protein in human cancer correlates with moderate/poor tumor differentiation.
Jiao W,Huei-Min Lin,Jashodeep Datta,Till Braunschweig,Joon-Yong Chung,Stephen M. Hewitt,Sushil G. Rane +6 more
TL;DR: It is proposed that RB inactivation, via aberrant nucleocytoplasmic transport, may disrupt normal cell differentiation programs and accelerate the cancer process, and is evidence that tumor cells modulate the protein transport machinery thereby making theprotein transport process a viable therapeutic target.
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A 165-base pair sequence between the dihydrofolate reductase gene and the divergently transcribed upstream gene is sufficient for bidirectional transcriptional activity.
TL;DR: A 165-base pair fragment from -111 to +54 relative to the dihydrofolate reductase initiation site was shown to be sufficient for transcriptional activity in either direction, suggesting that expression of the two divergent genes is regulated by a bidirectional promoter that may use common regulatory elements.