Sentence examples for mice we asked from inspiring English sources

Using these mice we asked where is collagen actively transcribed and secondly, what is the role of CCN2 in AAN.

Based upon the observations in mice, we asked whether monomeric TRAP is expressed in human adipose tissue, and whether it is over-expressed in obese patients.

Given the broad down-regulation of the Stat1 phosphorylation response to cytokines in lpr mice, we asked whether this lead to functional consequences in the cognate cells.

Given the defects in lymphoid populations observed in ezrin−/− mice, we asked if there is compensatory upregulation of moesin and radixin.

To identify the tissues that oxidized WAT-derived FFA in KO mice, we asked whether defective MA in BAT triggered 'Beige' cell [ 9] development in WAT.

Given the widespread differentiation defect of Sst+ cortical interneurons and the associated changes in dendritic inhibition observed in Lhx6 hypomorphic mice, we asked whether these animals develop seizures.

Given the enhanced pathological angiogenic responses in β3-null mice [12] we asked whether endothelial Rac1 was differentially required in tumor angiogenesis in adult wild-type or β3-null mice.

As neither migration defects nor cell death cause the reduced number of hippocampal neurons in Ngn2 null mice [20], we asked if Ngn2 is necessary for production of hippocampal granule neuroblasts.

Since pluripotent mEpiSC cells were derived from epiblast cells of E6.5 mouse embryos, we asked whether the H3K4me3 landscape of mEpiSCs in vitro was similar to that of E6.5 epiblast in vivo.

Because defects in cell cycle arrest and apoptosis of renal tubular epithelial cells occur in PKD, and in light of earlier reports that polycystin-1 upregulates p21 and that the cyclin-dependent kinase inhibitor roscovitine arrests progression in a mouse model, we asked whether (1) p21 deficiency might underlie ADPKD and (2) the mechanism of the salutary roscovitine effect on PKD involves p21.

To further dissect the role of miR-21 in mouse SLE, we asked whether transcription of miR-21 gene is activated in lupus by comparing the expression of pri-miR-21 in CD19+ B cells isolated from 9 months old B6.Sle123 and age/gender-matched B6. qRT-PCR analysis revealed up-regulation of pri-miR-21 transcript in B cells from lupus mice compared to controls (Fig 1D).