F
Fulu Liu
Researcher at Washington University in St. Louis
Publications - 26
Citations - 5071
Fulu Liu is an academic researcher from Washington University in St. Louis. The author has contributed to research in topics: Bone marrow & Haematopoiesis. The author has an hindex of 19, co-authored 26 publications receiving 4734 citations. Previous affiliations of Fulu Liu include Harvard University & University of Texas Health Science Center at San Antonio.
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Journal ArticleDOI
The origin and evolution of mutations in acute myeloid leukemia.
John S. Welch,Timothy J. Ley,Daniel C. Link,Christopher A. Miller,David E. Larson,Daniel C. Koboldt,Lukas D. Wartman,Tamara Lamprecht,Fulu Liu,Jun Xia,Cyriac Kandoth,Robert S. Fulton,Michael D. McLellan,David J. Dooling,John W. Wallis,Ken Chen,Chris Harris,Heather Schmidt,Joelle Kalicki-Veizer,Charles Lu,Qunyuan Zhang,Ling Lin,Michelle O'Laughlin,Joshua F. McMichael,Kim D. Delehaunty,Lucinda Fulton,Vincent Magrini,Sean McGrath,Ryan Demeter,Tammi L. Vickery,Jasreet Hundal,Lisa Cook,Gary W. Swift,Jerry P. Reed,Patricia A. Alldredge,Todd Wylie,Jason Walker,Mark A. Watson,Sharon Heath,William D. Shannon,Nobish Varghese,Rakesh Nagarajan,Jacqueline E. Payton,Jack Baty,Shashikant Kulkarni,Jeffery M. Klco,Michael H. Tomasson,Peter Westervelt,Matthew J. Walter,Timothy A. Graubert,John F. DiPersio,Li Ding,Elaine R. Mardis,Richard K. Wilson +53 more
TL;DR: The data suggest that most of the mutations found in AML genomes are actually random events that occurred in HSPCs before they acquired the initiating mutation; the mutational history of that cell is "captured" as the clone expands.
Journal ArticleDOI
G-CSF potently inhibits osteoblast activity and CXCL12 mRNA expression in the bone marrow
Craig L. Semerad,Matthew J. Christopher,Fulu Liu,Brenton Short,Paul J. Simmons,Ingrid G. Winkler,Jean-Pierre Levesque,Jean Chappel,F. Patrick Ross,Daniel C. Link +9 more
TL;DR: Data suggest a model in which G-CSF, through an indirect mechanism, potently inhibits osteoblast activity resulting in decreased CXCL12 expression in the bone marrow, which ultimately leads to HPC mobilization.
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Impaired Production and Increased Apoptosis of Neutrophils in Granulocyte Colony-Stimulating Factor Receptor–Deficient Mice
TL;DR: A role for the G-CSFR as a major regulator of granulopoiesis in vivo is confirmed and evidence is provided that G- CSFR-independent mechanisms of granutrophil survival must exist.
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G-CSF Is an Essential Regulator of Neutrophil Trafficking from the Bone Marrow to the Blood
TL;DR: It is shown that under basal conditions granulocyte colony-stimulating factor (G-CSF) is an essential regulator of neutrophil release from the bone marrow, and evidence is provided suggesting that downregulation of stromal cell-derived factor 1 expression in theBone marrow may represent such a signal.
Journal ArticleDOI
Expression of the G-CSF receptor in monocytic cells is sufficient to mediate hematopoietic progenitor mobilization by G-CSF in mice
TL;DR: Expression of the G- CSF receptor on bone marrow monocytes is sufficient to trigger HSC mobilization in response to G-CSF, in part via effects on osteoblast lineage cells.