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William E. Dowdle
Researcher at University of California, San Francisco
Publications - 22
Citations - 2063
William E. Dowdle is an academic researcher from University of California, San Francisco. The author has contributed to research in topics: Biology & Immunology. The author has an hindex of 12, co-authored 15 publications receiving 1710 citations. Previous affiliations of William E. Dowdle include Novartis & Harvard University.
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Journal ArticleDOI
Kif3a constrains beta-catenin-dependent Wnt signalling through dual ciliary and non-ciliary mechanisms.
TL;DR: It is shown that the primary cilium restricts the activity of the canonical Wnt pathway in mouse embryos, primary fibroblasts, and embryonic stem cells, and that unciliated cells activate transcription only in response to Wnt stimulation, but do so much more robustly than ciliated cells.
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Selective VPS34 inhibitor blocks autophagy and uncovers a role for NCOA4 in ferritin degradation and iron homeostasis in vivo
William E. Dowdle,Beat Nyfeler,Jane Nagel,Robert Elling,Shanming Liu,Ellen Triantafellow,Suchithra Menon,Zuncai Wang,Ayako Honda,Gwynn Pardee,John Cantwell,Catherine Luu,Ivan Cornella-Taracido,Edmund Harrington,Peter Fekkes,Hong Lei,Qing Fang,Mary Ellen Digan,Debra Burdick,Andrew F. Powers,Stephen B. Helliwell,Simon D’Aquin,Julie Bastien,Henry Wang,Dmitri Wiederschain,Jenny Kuerth,Philip Bergman,David Schwalb,Jason R. Thomas,Savuth Ugwonali,Fred Harbinski,John A. Tallarico,Christine D. Wilson,Vic E. Myer,Jeffery A. Porter,Dirksen E. Bussiere,Peter Finan,Mark Labow,Xiaohong Mao,Lawrence G. Hamann,Brendan D. Manning,Reginald Valdez,Thomas B. Nicholson,Markus Schirle,Mark Knapp,Erin P. Keaney,Leon Murphy +46 more
TL;DR: a4−/− mice exhibit a profound accumulation of iron in splenic macrophages, which are critical for the reutilization of iron from engulfed red blood cells, and a previously unappreciated role for autophagy and NCOA4 in the control of iron homeostasis in vivo is revealed.
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ERK2 but Not ERK1 Induces Epithelial-to-Mesenchymal Transformation via DEF Motif-Dependent Signaling Events
TL;DR: It is demonstrated that ERK2 but not ERK1 signaling is necessary for Ras-induced epithelial-to-mesenchymal transformation (EMT), and an apparent critical role for ERK 2 DEF motif signaling during tumorigenesis is the regulation of Fra1 and the subsequent induction of ZEB1/2, suggesting a potential therapeutic target for Ras.
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Disruption of a Ciliary B9 Protein Complex Causes Meckel Syndrome
William E. Dowdle,Jon F. Robinson,Andreas Kneist,M. Salomé Sirerol-Piquer,Suzanna G.M. Frints,Kevin C. Corbit,Norran A. Zaghloul,Norran A. Zaghloul,Gesina van Lijnschoten,Leon Mulders,Dideke E. Verver,Dideke E. Verver,Klaus Zerres,Randall R. Reed,Tania Attié-Bitach,Colin A. Johnson,José Manuel García-Verdugo,Nicholas Katsanis,Carsten Bergmann,Jeremy F. Reiter +19 more
TL;DR: In this paper, the role of the third B9 protein, B9d1, was examined and the p.Ser101Arg mutation abrogated the ability of b9d2 to interact with Mks1, further suggesting that the mutation compromised B9D2 function.
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Small-Molecule Modulation of TDP-43 Recruitment to Stress Granules Prevents Persistent TDP-43 Accumulation in ALS/FTD
Mark Y. Fang,Sebastian Markmiller,Anthony Q. Vu,Ashkan Javaherian,William E. Dowdle,Philippe Jolivet,Paul J. Bushway,Nicholas A. Castello,Ashmita Baral,Michelle Y. Chan,Jeremy W. Linsley,Drew Linsley,Mark Mercola,Mark Mercola,Steven Finkbeiner,Eric Lécuyer,Joseph W. Lewcock,Gene W. Yeo +17 more
TL;DR: It is proposed that compounds with planar moieties represent a promising starting point to develop small-molecule therapeutics for treating ALS/FTD and transient SG formation contributes to persistent accumulation of TDP-43 into cytoplasmic puncta.