A macrophage colony-stimulating factor receptor-green fluorescent protein transgene is expressed throughout the mononuclear phagocyte system of the mouse.
By R. T. Sasmono, D. Oceandy, J. Pollard, W. Tong, P. Pavli, B. Wainwright, Michael C. Ostrowski, S. R. Himes, David A. Hume. Blood, 2003
656 citations recorded by the source corpus.
Subfields: Immunology, Molecular Biology
View Paper: https://www.semanticscholar.org/paper/555b29e3735903b6bfe26995206b8707927a7d64
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In Immunology
In Molecular Biology
- J. Pollard
- Binzhi Qian
- Jiu-feng Li
- E. Stanley
- A. Gottfried-Blackmore
- J. Condeelis
- Kate Schroder
- Bruce S. McEwen
Citations in the corpus
- Macrophages regulate the angiogenic switch in a mouse model of breast cancer. (2006, background): “PyMT mice were used because the CSF-1R promoter is specifically expressed in macrophages (22).”
- Tumour-educated macrophages promote tumour progression and metastasis (2004, background): “However, recent advances that allow macrophages to be marked in vivo”
- Microglia derived from aging mice exhibit an altered inflammatory profile (2007, methodology): “In the present study, we provide evidence from a novel ex vivo approach to study microglia contribution to the aging process, using flow cytometry to purify viable microglia from fms-EGFP (Sasmono et al., 2003) mice and real-time-PCR to quantify the mRNA expression of inflammatory cytokines.”
- Osteal Tissue Macrophages Are Intercalated throughout Human and Mouse Bone Lining Tissues and Regulate Osteoblast Function In Vitro and In Vivo1 (2008, background): “Confocal microscopy assessment of bone surfaces collected from MacGreen mice (in which the csf1r promoter drives the expression of the enhanced GFP (eGFP), resulting in eGFP macrophages and other myeloid cells (14)), showed coexpression of eGFP and the F4/80 Ag within the endosteum (Fig.”
- A Distinct Macrophage Population Mediates Metastatic Breast Cancer Cell Extravasation, Establishment and Growth (2009, methodology): “Tg(Csf1r-EGFP)Hume mice have been previously reported to have the whole mononuclear phagocyte system labeled [31] and were remade on the FVB background FVB.”
- Blood monocytes: development, heterogeneity, and relationship with dendritic cells. (2009, background): “During the past few years, several teams have developed strategies for studying in vivo the differentiation, recruitment, and functions of blood monocytes using adoptive transfer and intravital studies (15, 23).”
- Microglia induce motor neuron death via the classical NF-κB pathway in amyotrophic lateral sclerosis (2014, neutral): “As shown by MacGreen reporter mice that express GFP under the regulation of the c-fms promoter, CSF-1R is expressed throughout the mononuclear phagocyte system of the mouse, but only microglia express CSF-1R in the postnatal mouse brain (Erblich et al., 2011; Sasmono and Williams, 2012; Sasmono et a”
- Trophic macrophages in development and disease (2009, background): “In some tissues, they constitute 10–20% of all cells — for example, microglial cells in the brain and Kupffer cells in the liver — whereas in other tissues, such as at the musculo–skeletal junctions, they are rar”
- Microglia shape adult hippocampal neurogenesis through apoptosis-coupled phagocytosis (2010, methodology): “Animals: Wild type (C57BL/6) or transgenic nestin-GFP (Mignone et al., 2004), nestin-CFPNuc (Encinas et al., 2006), fms-EGFP (Sasmono et al., 2003), POMC-EGFP (Overstreet et al., 2004) or hGFAP-GFP (Zhuo et al., 1997) mice were used in this study.”
- CSF-1 receptor signaling in myeloid cells. (2014, background): “Maximal CSF-1R expression in differentiated monocytes/macrophages requires a highly conserved 330 bp sequence enhancer element located in the 30 end of intron 2, known as Fms-intronic regulatory element (FIRE), which also has reverse promoter activity (Himes et al. 2001; Sasmono et al. 2003; Laslo e”
- Direct visualization of macrophage-assisted tumor cell intravasation in mammary tumors. (2007, background): “14) and Lys-GFP and c-fms (CSF-1R)-GFP mice were described previously (15, 16).”