L
Lesley F Drynan
Researcher at Laboratory of Molecular Biology
Publications - 24
Citations - 2457
Lesley F Drynan is an academic researcher from Laboratory of Molecular Biology. The author has contributed to research in topics: Fusion gene & Haematopoiesis. The author has an hindex of 18, co-authored 24 publications receiving 2293 citations.
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Journal ArticleDOI
Transcription factor RORα is critical for nuocyte development
See Heng Wong,See Heng Wong,Jennifer A. Walker,Helen E. Jolin,Lesley F Drynan,Emily Hams,Ana Camelo,Jillian L. Barlow,Daniel R. Neill,Daniel R. Neill,Veera Panova,Ute Koch,Freddy Radtke,Clare S. Hardman,You Yi Hwang,Padraic G. Fallon,Padraic G. Fallon,Andrew N J McKenzie +17 more
TL;DR: It is found that nuocytes arose in the bone marrow and differentiated from common lymphoid progenitors, which indicates they are distinct, previously unknown members of the lymphoid lineage.
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Innate IL-13–producing nuocytes arise during allergic lung inflammation and contribute to airways hyperreactivity
Jillian L. Barlow,Agustin Bellosi,Clare S. Hardman,Lesley F Drynan,See Heng Wong,James Cruickshank,Andrew N. J. McKenzie +6 more
TL;DR: These findings identify nuocytes as a novel cell type in allergic lung inflammation and an innate source of IL-13 that can directly induce AHR in the absence ofIL-13-producing CD4(+) T cells.
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A p53-dependent mechanism underlies macrocytic anemia in a mouse model of human 5q– syndrome
Jillian L. Barlow,Lesley F Drynan,Duncan R. Hewett,Luke R Holmes,Silvia Lorenzo-Abalde,Alison L Lane,Helen E. Jolin,Richard Pannell,Angela J Middleton,See Heng Wong,Alan J. Warren,Alan J. Warren,James S. Wainscoat,Jacqueline Boultwood,Andrew N. J. McKenzie +14 more
TL;DR: This mouse model suggests that a p53-dependent mechanism underlies the pathophysiology of the 5q– syndrome, and rescues the progenitor cell defect, restoring common myeloid progensitor and megakaryocytic-erythroid progenitors and hematopoietic stem cell bone marrow populations.
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Uncoupling of GTP hydrolysis from eIF6 release on the ribosome causes Shwachman-Diamond syndrome
Andrew J. Finch,Christine Hilcenko,Nicolas Basse,Lesley F Drynan,Beatriz Goyenechea,Tobias F. Menne,África González Fernández,Paul J. Simpson,Clive D'Santos,Mark J. Arends,Jean Donadieu,Christine Bellanné-Chantelot,Michael Costanzo,Charles Boone,Andrew N. J. McKenzie,Stefan M.V. Freund,Alan J. Warren +16 more
TL;DR: These findings establish a direct role for SBDS and EFL1 in catalyzing the translational activation of ribosomes in all eukaryotes, and define SDS as a ribosomopathy caused by uncoupling GTP hydrolysis from eIF6 release.
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The LMO2 T-cell oncogene is activated via chromosomal translocations or retroviral insertion during gene therapy but has no mandatory role in normal T-cell development.
TL;DR: It is concluded that there is no mandatory role for LMO2 in lymphoid development, implying that its specific role in T-cell tumorigenesis results from a reprogramming of gene expression after enforced expression inT-cell precursors.