Transepithelial resistance was not altered in Tg and Ko mice, indicating that tight junctions were not affected.
A similar distribution was observed in K5cre-CMVcaNrf2 mindicatingathat tighttight junction permeability is not grossly affected (Fig 5B).
However, most of these lines could not produce iPSC-mice by tetraploid complementation except chimeric mice, indicating that they were not entirely pluripotent.
Tax was unable to inhibit p53 in p65−/− mice, indicating that this effect was NF-kappaB dependent.
Importantly, T cell function was compromised in Jnk1Jnk2 double heterozygous mice, indicating that JNK1 and JNK2 play similar roles in regulating T cell function.
The expression levels of leptin mRNA approximately identify with body fat rate in mice, indicating that leptin resistance occurs in the obese mice fed with higher soybean oil.
However, we did detect both at the mRNA and protein level minor induction of UGT1A1 in hUGT1/Car−/− mice, indicating that an alternative mechanism exists.
We also observed higher percentages of myeloid-derived cell populations within tumors in Fas-deficient mice, indicating that tumor stromal destruction was dependent on the Fas death receptor.
PE27 also induced IFN-γ-producing memory T cell responses in Mtb-infected mice, indicating that PE27 contributes to Th1-polarization.
Moreover, these same four determinants controlled PVM expression in a second strain of mice, indicating that the underlying mechanism is operational in mice of different genetic backgrounds.
We find that approximately 30% of α-catulin-GFPc-kit cells give long-term multilineage reconstitution of irradiated mice, indicating that α-catulin-GFPc-kit cells are comparable in HSC purity to cells obtained using the best markers currently available.
