To identify protein biomarkers of nanomaterials in mice, we analyzed changes in the levels of plasma proteins following treatment with nSP70 by using 2D-DIGE.
Using the B16 melanoma model and the inducible depletion of CD11c+ cells in CD11c.diphtheria toxin receptor (DTR) mice, we analyzed the interaction between tumor-resident cDCs and engineered T cells expressing the melanoma-specific TRP-2 TCR.
To further characterize the bone pathology of knock-in mice we analyzed bone morphology by micro CT imaging.
As we found an osteopenic phenotype in adult Cthrc1-null mice, we analyzed bone in adult Cthrc1 transgenic mice.
To determine the reason for extended mating intervals in the female mice, we analyzed the regularity of their estrous cycles.
To investigate why tumors were larger in HRG-deficient mice, we analyzed the proliferative and apoptotic status, as well as the vascularization, of the dissected tumors.
To increase our understanding of the impaired inflammatory response observed in PLCγ2−/− mice, we analyzed T cell activation after induction of the disease.
To investigate the molecular mechanisms of polyp formation in ApcΔ14/+FHL2−/− mice, we analyzed expression of β-catenin and its targets cyclin D1 and c-myc in tumors.
Because APP derived polypeptides are significantly changed in APPYG/YG mice, we analyzed whether these mutant mice show abnormalities in brain organization.
Thus, to analyze if autophagic processes were also disrupted in the knock-in mice, we analyzed the expression of the LC3B-II protein.
Because of the lethality of C57/BL6J backcrossed null mutant mice, we analyzed heterozygous Scrapper gene-deficient mice [SCR ] using behavioral test battery.
