To investigate further how angiogenesis functions in CD146EC-KO mice, we performed an aortic ring assay.
To determine the accelerated proliferation in RNF13-/ mice, we performed BrdU and MyoD double staining (Fig. 2H).
In order to further assess the development of metastatic burden in individual mice, we performed longitudinal whole body BLI in each control and treated mouse.
To quantitatively determine the uptake of [18F]FTC-146 in WT versus S1R-KO mice, we performed ex vivo biodistribution studies 25 min post-injection of tracer (Fig. 3).
For genotyping of importin α7−/− mice, we performed RT-PCR with RNA isolated from tail biopsies.
To investigate the blood glucose regulatory ability of IRE1α CKO mice, we performed oral glucose tolerance test (OGTT).
To further confirm reduced phosphorylation of p70S6K in Tg2576 compared to WT mice we performed immuno-fluorescence confocal microscopy.
To examine the whole-body glucose utilization in Leptin145E/145E mice, we performed the oral glucose tolerance test (OGTT).
To distinguish between hemizygous and homozygous rhodopsin knockout mice, we performed Southern blot analysis based on a previous protocol [67].
To characterize the cellular expression profiles of hCD4 and hCCR5 in these mice, we performed flow cytometry analysis by co-staining for mouse CD4, hCD4, and hCCR5.
To rule out a general hypo-locomotion in running mice, we performed a home cage activity measurement in another cohort of mice.
