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Previous works in mice also indicated high expression of TE in germlines.
The lack of triglyceride accumulation in T3-treated mice also indicated the possibility of an enhanced fatty acid oxidation which overriding the effect of DNL.
In addition, RELB deficient mice exhibited a multifocal, mixed inflammatory cell infiltration in several organs [ 53] and fibroblasts from RELB deficient mice, also indicated an important role of RELB as transcription suppressor limiting the expression of proinflammatory mediators [ 54].
The increased number of intestinal granulomas in IL-6−/− mice also indicated potentiation of type 2 responses early in infection, as these are foci of alternatively activated macrophages, which form in an IL-4Rα-dependent manner [ 22].
A systematic examination of pain-related behaviors in BDNF heterozygote mutant mice also indicated that even reduced gene dosage of this important factor can lead to deficits in acute noxious heat sensitivity and reduced pain behaviors, e.g. in the formalin test (MacQueen et al., 2001).
Similar(55)
Furthermore, the levels of IFN-γ were similarly decreased by day 22 in both WT and CKO mice, also indicating that EGR-2 deficient mice had normal resolution of the response.
The complete silencing of the VpreB/λ5 locus observed in splenic B cells of double-deficient mice also indicates that silencing is a prerequisite for immature B cells to exit from the bone marrow compartment.
Transgenic and knockout mice also indicate the neuroprotective role of GluN3A (Nakanishi et al., 2009).
Studies in mice also indicate that there is a difference between gene deletion and catalytic site mutation.
The lack of an overt phenotype in these mice also indicates that CCT domain inhibitors may be well tolerated.
The remarkable susceptibility of some DO mice also indicates that genetic material from founder strains enhances susceptibility to M. tuberculosis.
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