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However, while the administration of human fibrocytes to severe combined immunodeficiency (SCID) mice requires coadministration of bleomycin to result in pathology [ 12], requirement for injury in the accumulation of CD45+Col-I+ in the TGF-β1-exposed murine lung has not been shown.
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This prompted the current study, wherein the genetic profiling of flaxseed in murine lungs has been evaluated.
These data were not entirely surprising, because recruitment of fibrocytes to murine lungs has been shown to be mediated by other receptors including chemokine CXC motif receptor (CXCR 4, CCR2 and CCR5 [ 28- 30].
Interestingly, the immunofluorescence of vinculin showed that the ACTN4 KD murine lung fibroblasts had large and long focal adhesion sites at the edge of cell and the cell body had a few focal adhesion sites (Fig. 3A).
Murine lung tumors have been shown to contain a high frequency of K-ras mutation in codon 61 [37].
We hypothesized that mCLCA5 protein is expressed in highly select areas of the naive murine lung, since it has only been found on the mRNA level in total lung extracts so far.
LEC (murine lung endothelial cells) have been described previously [94]; HDMEC (human dermal microvascular endothelial cells) and NHDF (Normal human dermal fibroblasts) primary cultures were purchased from PromoCell (Heidelberg, Germany. HA-SMC and HC-SMC (human normal smooth muscle cells) primary cultures were purchased from ScienCell Research Laboratories (Carlsbad, CA).
Here, we report that Ang-1 appears important in normal murine lung development, and have established its tissue-level expression and localization patterns at key time-points.
Combined liquid chromatography-tandem MS (LC-MS/MS) has been used to analyze proteins released into conditioned media, surface proteins and whole-cell lysates of murine lung cancer cells that have undergone epithelial-mesenchymal transition (EMT, a process that allows tumor cells with an epithelial phenotype to convert to mesenchymal cells).
Utilising subcutaneous murine lung cancer models, we have previously shown that CCL19 promotes IFN- γ-dependent antitumour responses (Hillinger et al, 2003).
We queried murine lung fibroblasts in which ACTN4 has been stably and significantly downregulated [9].
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