J
James Kim
Researcher at University of Texas Southwestern Medical Center
Publications - 131
Citations - 6585
James Kim is an academic researcher from University of Texas Southwestern Medical Center. The author has contributed to research in topics: Reading comprehension & Reading (process). The author has an hindex of 40, co-authored 121 publications receiving 5808 citations. Previous affiliations of James Kim include University of Texas at Dallas & University of Rochester.
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Journal ArticleDOI
Coaxial Stacking of Helixes Enhances Binding of Oligoribonucleotides and Improves Predictions of RNA Folding
Amy E. Walter,Douglas H. Turner,James Kim,Matthew H. Lyttle,Peter Müller,David H. Mathews,Michael Zuker +6 more
TL;DR: An RNA model system consisting of an oligomer binding to a 4-nt overhang at the 5' end of a hairpin stem provides thermodynamic parameters for helix-helix interfaces and predictions of 11 RNA secondary structures improve from 67 to 74% accuracy by inclusion of similar stacking contributions.
Journal ArticleDOI
Itraconazole, a Commonly Used Antifungal that Inhibits Hedgehog Pathway Activity and Cancer Growth
James Kim,Jean Y. Tang,Jean Y. Tang,Ruoyu Gong,Jynho Kim,John J. Lee,Karl V. Clemons,Curtis R. Chong,Kris S. Chang,Mark Fereshteh,Dale R. Gardner,Tannishtha Reya,Jun O. Liu,Ervin H. Epstein,David A. Stevens,Philip A. Beachy +15 more
TL;DR: Mechanistically, itraconazole appears to act on the essential Hh pathway component Smoothened by a mechanism distinct from that of cyclopamine and other known SMO antagonists, and prevents the ciliary accumulation of SMO normally caused by Hh stimulation.
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Hedgehog/Wnt feedback supports regenerative proliferation of epithelial stem cells in bladder
Kunyoo Shin,John H. Lee,Nini Guo,James Kim,Agnes Lim,Lishu Qu,Indira U. Mysorekar,Philip A. Beachy +7 more
TL;DR: It is shown in mice that the proliferative response to bacterial infection or chemical injury within the bladder is regulated by signal feedback between basal cells of the urothelium and the stromal cells that underlie them, which provides a conceptual framework for injury-induced epithelial regeneration in endodermal organs.
Journal ArticleDOI
Itraconazole and Arsenic Trioxide Inhibit Hedgehog Pathway Activation and Tumor Growth Associated with Acquired Resistance to Smoothened Antagonists
James Kim,Blake T. Aftab,Blake T. Aftab,Jean Y. Tang,Jean Y. Tang,Daniel H. Kim,Alexander Lee,Alexander Lee,Melika Rezaee,Jynho Kim,Baozhi Chen,Emily M. King,Alexandra Borodovsky,Gregory J. Riggins,Ervin H. Epstein,Philip A. Beachy,Charles M. Rudin +16 more
TL;DR: It is reported that itraconazole and arsenic trioxide, two agents in clinical use that inhibit Hedgehog signaling by mechanisms distinct from that of current Smoothened antagonists, retain inhibitory activity in vitro in the context of all reported resistance-conferring Smothened mutants and GLI2 overexpression.
Journal ArticleDOI
Arsenic antagonizes the Hedgehog pathway by preventing ciliary accumulation and reducing stability of the Gli2 transcriptional effector
TL;DR: Arsenic could be tested rapidly as a therapeutic agent in malignant diseases associated with Hh pathway activation and could be particularly useful in such diseases that are inherently resistant or have acquired resistance to cyclopamine mimics.