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Melanosome transport defects in ashen mice are caused by a mutation in the Rab27a locus [14].

This comparison lends further support to our hypothesis that the differentially expressed genes in our antibiotic treated mice are caused by greatly reduced microbial stimuli.

Moreover, tumorous β-cells isolated from RIP1-Tag2 tumors did not express VEGFR-1 mRNA, in contrast to isolated blood endothelial cells from the same tumors (Figure 2a), making it likely that potential effects of transgenic expression of VEGF-B on tumor progression in RIP1-Tag2 mice are caused by paracrine stimulation.

This result ruled out the possibility that the respiratory alterations observed in DMSXL mice are caused by their small size.

Based on these results, we hypothesized that accelerated inflammation and fibrosis observed in Fra-1∆/∆ mice are caused by enhanced inflammatory and fibrotic gene expression.

However, whether the hypomyelination and seizure phenotypes in BACE1 -/- mice are caused by the lack of BACE1 activity in the adult or during embryonic or postnatal development is currently unknown.

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We took two lists of genes that when knocked out in mice are causing the phenotypes of 'embryonic growth arrest' and 'abnormal kidney physiology' based on the MGI-MP ontology (18) terms 1730 and 2136 respectively.

Next, we tested whether L435-3-mediated L435-3-mediated L435-3-mediatedn minhibitionused by increased expressiof of IAVereplication

These results strongly suggest that the neonatal death of jsap1-deficient mice is caused by defects in the nervous system.

These results demonstrate that the decreased fibrosis seen in mutant mice is caused directly by the increase in IL-10.

The obese phenotype of Leptinob/ob mice is caused by mutations in either the coding region (ob 1J)) [6] or the 5' non-coding region (ob 2J)) [7] of mouse Leptin gene.

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