Sentence examples for mice contributes to from inspiring English sources

Based on these results, it is suggested that overexpression of GABAA receptor β2 subunit in BALB/cByJ mice relative to C57BL/6j mice contributes to the dysfunction in GABAA transmission in regions of brain known to regulate responses to stress.

ESL degradation in apoE deficient mice contributes to reduced increased urinary protein excretion without significant changes in renal morphology.

Taken together, these data implicate an important role for TIEG1 in regulating the expression and activity of Runx2 in osteoblasts and suggest that decreased expression of Runx2 in TIEG1 KO mice contributes to the observed osteopenic bone phenotype.

However, it is to be noted that while the ovary as the primary site of P4 synthesis in pregnant mice contributes to CRH secretion, CRH like P4 is mainly produced by the placenta during late gestation in humans [47].

These results suggest that the high corticosterone level of ZT2 in the RF mice contributes to the corresponding peak expression of tyrosine aminotransferase, and likely also the initial peak of Cyp7A1 expression.

A recent study has also provided evidence that reduced hippocampal levels of MARCKS, and thus PIP2, in mice contributes to age-related cognitive loss (Trovò et al., 2013).

Determine if impaired intestinal barrier function and low-grade chronic inflammation in Zip14 KO mice contribute to ZIP14-associated parkinsonism.

Could the excessive incidence of tumorigenesis in p53-deficient mice contribute to our understanding of the threshold vs nonthreshold issue in genotoxic carcinogenesis?

Moreover, we investigate whether the deregulated hemostasis in HRG-deficient mice contribute to the elevated angiogenic switch, previously reported in these mice.

Taken together, the data indicated that both impaired BMMSCs and activated osteoclast activity in CD4+CD25−CD45RB+hi T cell-treated OVX-immunocompromised mice contributed to the osteoporosis phenotype.

Enhanced cathepsin expression and activity in cystatin C-deficient mice contributed to the progression of dysplasia by altering premalignant tissue epithelial proliferation, apoptosis, and neovascularization.