Using OEG and DRG from L1 mutant mice we found that L1 expression does not contribute to OEG growth promotion.
In Oxtr −/− mice, we found that the total number of BrdU+ cells was significantly increased by hM3Dq/CNO-based approach (Fig. 8d, e).
Following a combination of two mucosal and two systemic vaccinations of mice, we found significant enhancement of both local and systemic antibodies as well as cytokine responses.
When capillary-like networks engineered on amnion membranes were transplanted into mice, we found blood cells inside of the lumen of the transplanted capillary-like structure.
In a xenotransplantation model using NOD/SCID mice, we found that transduced CD34+ cells could repopulate irradiated recipient animals, as measured by CD25 expression.
Using genetically engineered mice, we found that Rai1 preferentially occupies DNA regions near active promoters and promotes the expression of a group of genes involved in circuit assembly and neuronal communication.
When the stratum radiatum (SR) was stimulated in slices from injured mice, we found decreased depolarization in SR and increased hyperpolarization in stratum oriens (SO), together with a decrease in the percentage of pyramidal neurons firing stimulus-evoked action potentials.
As previously reported, in certain aged mice we found prominent infiltration of adipocytes concentrated in the distal metaphysis of femurs, which resulted in partial perturbation of the overall stromal parenchyma (not shown).
In line with reports correlating Aβ reduction with functional and cognitive improvement16,19,33,34, in NSC mice we found decreased plaques and lower total Aβ42, the main component of neuritic plaques.
Consistent with the results from Oxtr −/− mice, we found a significant reduction of the total of BrdU+ cells in Oxtr f/f mice with AAV-Cre-GFP injections compared with those injected with of AAV-GFP (Supplementary Fig. 8d, e).
In Bmi1-derived cells from Bmi1CreERT/+R26YFP/+ PQ-treated mice, we found upregulation of several differentiation-related genes, particularly of cardiomyocyte- and myofibroblast-related genes (Fig. 4c), which confirmed ChIP-seq data.
