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David A. Hume
Researcher at University of Queensland
Publications - 612
Citations - 66127
David A. Hume is an academic researcher from University of Queensland. The author has contributed to research in topics: Macrophage & Macrophage colony-stimulating factor. The author has an hindex of 113, co-authored 573 publications receiving 59932 citations. Previous affiliations of David A. Hume include University of California, San Diego & University of Oxford.
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Journal ArticleDOI
Analysis of the impact of CSF-1 administration in adult rats using a novel Csf1r-mApple reporter gene
Katharine M. Irvine,Melanie Caruso,Michelle Ferrari Cestari,Gemma M. Davis,Sahar Keshvari,Anuj Sehgal,Clare Pridans,David A. Hume,David A. Hume +8 more
TL;DR: The Csf1r‐mApple rat is a novel tool enabling analysis of rat macrophages in situ by direct imaging and providing an additional phenotypesic marker to facilitate exploration of rat tissue macrophage phenotypic and functional heterogeneity.
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Experimental and bioinformatic characterisation of the promoter region of the Marfan syndrome gene, FBN1
Kim M. Summers,Nilesh J. Bokil,John M. Baisden,Malcolm J. West,Matthew J. Sweet,Liza J. Raggatt,David A. Hume +6 more
TL;DR: MG63 appears to be the optimal cell line for examining tissue-specific, biologically relevant promoter activity for FBN1, and the conserved promoter region was more active in MG63 cells than in non-FBN1-expressing lines but additional elements outside the proximal promoter are probably required for optimal tissue- specific expression.
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Regulation of urokinase plasminogen activator gene transcription in the RAW264 murine macrophage cell line by macrophage colony-stimulating factor (CSF-1) is dependent upon the level of cell-surface receptor.
TL;DR: It is demonstrated that the murine macrophage cell line RAW264 responds to CSF-1 with inducible phosphorylation of cytoplasmic proteins on tyrosine residues but fails to induce transcription of uPA, indicating that maintenance of elevated uPA transcription by CSf-1 requires new receptors emerging continuously on the cell surface.
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Absence of microglia promotes diverse pathologies and early lethality in Alzheimer’s disease mice
Sepideh Kiani Shabestari,Samuel Morabito,Emma Danhash,Amanda McQuade,Jessica Ramirez Sanchez,Emily Miyoshi,Jean Paul Chadarevian,Christel Claes,Morgan A. Coburn,Jonathan Hasselmann,J Hidalgo,Kayla Nhi Tran,Alessandra C. Martini,Winston Chang Rothermich,Jesse Pascual,Elizabeth Head,David A. Hume,Clare Pridans,Hayk Davtyan,Vivek Swarup,Mathew Blurton-Jones +20 more
TL;DR: In this article , microglia are strongly implicated in the development and progression of Alzheimer's disease (AD), yet their impact on pathology and lifespan remains unclear, and the authors utilize a CSF1R hypomorphic mouse to generate a model of AD that genetically lacks micro-glia.