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Gain- and loss-of-function strategies using transgenic over-expression and targeted ablation of candidate genes in in the mouse have provided important mechanistic insights into cardiovascular development, physiology and disease.
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Since SP-C is a marker for alveolar type II cells [ 28, 33], the promoter for this gene was used for transgenic over-expression of SCGB3A2 in the alveolar areas because in a previous study using the BLM-induced pulmonary fibrosis model, pulmonary fibrosis was reduced by intravenous administration of SCGB3A2 [ 16, 24].
The DEG transcripts showed higher expression in tolerant genotypes could be used for transgenic over-expression in sensitive genotypes of sorghum and related crops for increased tolerance to N-stress, which results in increased nitrogen use efficiency for sustainable agriculture.
As described, the model of islet dysmorphogenesis used for these studies was islet-specific Hnf6 transgenic over-expression.
Transgenic over-expression of human mutant genes has been extensively used to generate mouse models for human neurodegenerative disorders due to the need of over-expressing enough amount of the mutant protein in order to observe a phenotype.
Transgenic over-expression of defence peptide genes is potentially useful to engineer resistance of plants to relevant pathogens.
Transgenic over-expression of catalase in the peroxisome or nucleus did not extend mouse lifespan [18] [20].
Moreover, transgenic over-expression of Serpine1 in mice attenuates diet induced obesity.
Transgenic over-expression of Slfn4 in myeloid cells did not alter macrophage colony formation or proliferation in vitro.
Transgenic over-expression of calpastatin restored the vascular relaxation back to the normal levels.
Transgenic over-expression of calpastatin reduced ROS production and peroxynitrite formation in diabetic mice.
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