J
James K. Chen
Researcher at Stanford University
Publications - 142
Citations - 14257
James K. Chen is an academic researcher from Stanford University. The author has contributed to research in topics: Hedgehog signaling pathway & Smoothened. The author has an hindex of 49, co-authored 139 publications receiving 12853 citations. Previous affiliations of James K. Chen include Pacific Northwest National Laboratory & Harvard University.
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Journal ArticleDOI
Inhibition of Hedgehog signaling by direct binding of cyclopamine to Smoothened.
TL;DR: It is shown that cyclopamine can reverse the retention of partially misfolded Smo in the endoplasmic reticulum through binding-mediated effects on protein conformation, which suggests a role for small molecules in the physiological regulation of Smo.
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Effects of oncogenic mutations in Smoothened and Patched can be reversed by cyclopamine
Jussi Taipale,James K. Chen,Michael K. Cooper,Baolin Wang,Randall K. Mann,Ljiljana Milenkovic,Matthew P. Scott,Philip A. Beachy +7 more
TL;DR: It is shown that the plant-derived teratogen cyclopamine, which inhibits the Hh response, is a potential ‘mechanism-based’ therapeutic agent for treatment of these tumours.
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Structural basis for the binding of proline-rich peptides to SH3 domains
TL;DR: It is concluded that SH3 domains recognize proline-rich motifs possessing the left-handed type II polyproline (PPII) helix conformation, and these motifs appear to function as a molecular scaffold, promoting the formation of the PPII helix.
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Small molecule modulation of Smoothened activity.
TL;DR: It is demonstrated that SAG, a chlorobenzothiophene-containing Hh pathway agonist, binds to the Smo heptahelical bundle in a manner that antagonizes cyclopamine action, and four small molecules that directly inhibit Smo activity but are structurally distinct fromcyclopamine are identified.
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Medulloblastoma Growth Inhibition by Hedgehog Pathway Blockade
David M. Berman,Sunil S. Karhadkar,Andrew R. Hallahan,Joel I. Pritchard,Charles G. Eberhart,D. Neil Watkins,James K. Chen,Michael K. Cooper,Jussi Taipale,James M. Olson,Philip A. Beachy +10 more
TL;DR: This compound caused regression of murine tumor allografts in vivo and induced rapid death of cells from freshly resected human medulloblastomas, but not from other brain tumors, thus establishing a specific role for Hh pathway activity in medullOBlastoma growth.