Meanings of generated transgenic in English

To test the hypothesis, we generated transgenic mice with targeted expression of p52 in lymphocytes.

We generated transgenic mice dominantly expressing ATRAP in the renal tubules, including renal distal tubules.

Moreover, we generated transgenic marmosets in which the transgene was controlled by the tetracycline-inducible gene expression system.

We generated transgenic mice in which levels of bioactive ghrelin are increased in the stomach and circulation.

We have generated transgenic mice that express a trans-dominant-negative mutant of c-Jun (TAM-67) specifically in thymocytes.

We generated transgenic mice expressing a constitutively active VP16-LXRa protein from the aP2 promoter.

We generated transgenic mice expressing alpha-dystrobrevin-2a linked to a palmitoylation signal sequence and bred them onto the alpha-dystrobrevin-null and mdx backgrounds.

To examine this hypothesis, we next generated transgenic mice expressing ATRAP specifically in cardiomyocytes under control of the alpha-myosin heavy chain promoter.

To investigate the molecular mechanisms underlying these processes, we generated transgenic tobacco harboring the AK-6b gene under the control of a dexamethazone-inducible promoter.

To investigate the actions of gremlin on bone remodeling in vivo, we generated transgenic mice overexpressing gremlin under the control of the osteocalcin promoter.

We generated transgenic zebrafish animals expressing the photo-convertible fluorescent protein Kaede in ADt neurons and then photo-converted Kaede to label specifically the ADt neuron axons.

We previously generated transgenic Eker rats and identified coding sequences in the Tsc2 gene that are responsible for suppression of renal carcinogenesis in Eker rats.

Methods and results: To solve this problem, we have generated transgenic mice overexpressing intact p300 or mutant p300 in the heart.

Thus, we generated transgenic mice that express a GLUT2-loop domain, blocking the detection of glucose but leaving GLUT2-dependent glucose transport unaffected.

To investigate the role of IL-9 in vivo, we have generated transgenic mice in which IL-9 is expressed from its own promoter.

Methods and results: We generated transgenic mice with cardiac myocyte-restricted expression of Grx1-roGFP2 targeted either to the mitochondrial matrix or to the cytoplasm.