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Female mice express higher levels of glutaredoxin in certain CNS regions and downregulation of glutaredoxin using antisense oligonucleotides sensitizes them to l-BOAA toxicity seen as mitochondrial complex I loss.
This group demonstrated that due to defective insulin signaling, but independent of glucose and free fatty acids, macrophages from ob/ob mice express higher levels of SR-A and CD36 resulting in elevated cellular association with acetylated and oxidized LDL and increased cholesteryl ester formation [7].
Interestingly, a comparison of gene expression analysis between pre-autoimmune (NZB × NZW) F1 and MRL/lpr mice has suggested that mononuclear cells from (NZB × NZW) F1 female mice express higher levels of IFN-α and IFN-γ-inducible genes than the MRL/lpr mice [26].
Polyomavirus middle T transgenic mice express higher β1 in disordered structures than in normal acini at 10 weeks old.
Mouse studies showed that microglia from SOD1G93A ALS mice express higher levels of the prostaglandin E2 receptor (Di Giorgio et al, 2008; de Boer et al, 2014).
Macrophages derived from Fpr2 deficient mice express higher levels of the chemokine GPCR, CCR4, which in cooperation with CCR2 mediate a marked increase in macrophage chemotaxis in response to CCL2.
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OCPs from joints of TNF-Tg mice express high levels of VEGF-C.
In contrast, DGCs from HuD-Tg mice express high levels of this protein even in adult mice.
BCG-infected mice express high levels of the Th2 cytokines interleukin (IL -5 and IL -5 [ 7].
Figure 5A,B shows that compared with the majority of microglial cells in WT mice, which are IbaI+/CD39+, plaque-associated microglia in APPSw,Ind Tg mice express high levels of CD39 (CD39high, Fig. 5B,C1).
Thyroid C cells of rats and mice express high concentrations of GLP-1 receptors and respond to high concentrations of GLP-1 receptor agonists with excess calcitonin secretion and C-cell hyperplasia (65).
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