scholarly journals Generation of a Novel Transgenic Mouse Model for Bioluminescent Monitoring of Survivin Gene Activity in Vivo at Various Pathophysiological Processes

2010 ◽  
Vol 176 (4) ◽  
pp. 1629-1638 ◽  
Author(s):  
Fengzhi Li ◽  
Qiuying Cheng ◽  
Xiang Ling ◽  
Aimee Stablewski ◽  
Lei Tang ◽  
...  
Keyword(s):  
Mouse Model ◽  
Transgenic Mouse ◽  
Transgenic Mouse Model ◽  
Gene Activity ◽  
Survivin Gene ◽  
Bioluminescent Monitoring

scholarly journals Multimodal In Vivo Imaging of Tumorigenesis and Response to Chemotherapy in a Transgenic Mouse Model of Mammary Cancer

2015 ◽  
Vol 18 (4) ◽  
pp. 617-626 ◽  
Author(s):  
Jean-Louis Alberini ◽  
Raphaël Boisgard ◽  
Stéphanie Guillermet ◽  
Karine Siquier ◽  
Benoît Jego ◽  
...  
Keyword(s):  
Mouse Model ◽  
Transgenic Mouse ◽  
In Vivo Imaging ◽  
Mammary Cancer ◽  
Transgenic Mouse Model ◽  
Response To Chemotherapy

scholarly journals In Vivo Monitoring of Pancreatic β-Cells in a Transgenic Mouse Model

2006 ◽  
Vol 5 (2) ◽  
pp. 7290.2006.00007 ◽  
Author(s):  
Steven J. Smith ◽  
Hongbing Zhang ◽  
Anne O. Clermont ◽  
Alvin C. Powers ◽  
Dixon B. Kaufman ◽  
...  
Keyword(s):  
Mouse Model ◽  
Transgenic Mouse ◽  
Transgenic Mouse Model ◽  
Β Cells ◽  
Pancreatic Β Cells ◽  
In Vivo Monitoring

In Vivo Imaging of Lymph Node Migration of MNP- and 111In-Labeled Dendritic Cells in a Transgenic Mouse Model of Breast Cancer (MMTV-Ras)

2011 ◽  
Vol 14 (2) ◽  
pp. 183-196 ◽  
Author(s):  
Cristina Martelli ◽  
Manuela Borelli ◽  
Luisa Ottobrini ◽  
Veronica Rainone ◽  
Anna Degrassi ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Dendritic Cells ◽  
Lymph Node ◽  
Mouse Model ◽  
Transgenic Mouse ◽  
In Vivo Imaging ◽  
Transgenic Mouse Model

scholarly journals PRT-060318, a novel Syk inhibitor, prevents heparin-induced thrombocytopenia and thrombosis in a transgenic mouse model

Blood ◽  
2011 ◽  
Vol 117 (7) ◽  
pp. 2241-2246 ◽  
Author(s):  
Michael P. Reilly ◽  
Uma Sinha ◽  
Pierrette André ◽  
Scott M. Taylor ◽  
Yvonne Pak ◽  
...  
Keyword(s):  
Mouse Model ◽  
Transgenic Mouse ◽  
Immune Complex ◽  
Transgenic Mouse Model ◽  
Control Group ◽  
Platelet Factor ◽  
Heparin Induced Thrombocytopenia ◽  
Syk Inhibitor ◽  
Induced Aggregation

AbstractHeparin-induced thrombocytopenia (HIT) is a major cause of morbidity and mortality resulting from the associated thrombosis. Extensive studies using our transgenic mouse model of HIT have shown that antibodies reactive with heparin-platelet factor 4 complexes lead to FcγRIIA-mediated platelet activation in vitro as well as thrombocytopenia and thrombosis in vivo. We tested PRT-060318 (PRT318), a novel selective inhibitor of the tyrosine kinase Syk, as an approach to HIT treatment. PRT318 completely inhibited HIT immune complex-induced aggregation of both human and transgenic HIT mouse platelets. Transgenic HIT model mice were treated with KKO, a mouse monoclonal HIT-like antibody, and heparin. The experimental group received orally dosed PRT318, whereas the control group received vehicle. Nadir platelet counts of PRT318-treated mice were significantly higher than those of control mice. When examined with a novel thrombosis visualization technique, mice treated with PRT318 had significantly reduced thrombosis. The Syk inhibitor PRT318 thus prevented both HIT immune complex-induced thrombocytopenia and thrombosis in vivo, demonstrating its activity in HIT.

scholarly journals The cytoplasmic NPM mutant induces myeloproliferation in a transgenic mouse model

Blood ◽  
2010 ◽  
Vol 115 (16) ◽  
pp. 3341-3345 ◽  
Author(s):  
Ke Cheng ◽  
Paolo Sportoletti ◽  
Keisuke Ito ◽  
John G. Clohessy ◽  
Julie Teruya-Feldstein ◽  
...  
Keyword(s):  
Acute Myeloid Leukemia ◽  
Mouse Model ◽  
Transgenic Mice ◽  
Transgenic Mouse ◽  
Myeloid Leukemia ◽  
Gene Mutations ◽  
Transgenic Mouse Model ◽  
Acute Myeloid

Abstract Although NPM1 gene mutations leading to aberrant cytoplasmic expression of nucleophosmin (NPMc+) are the most frequent genetic lesions in acute myeloid leukemia, there is yet no experimental model demonstrating their oncogenicity in vivo. We report the generation and characterization of a transgenic mouse model expressing the most frequent human NPMc+ mutation driven by the myeloid-specific human MRP8 promoter (hMRP8-NPMc+). In parallel, we generated a similar wild-type NPM trans-genic model (hMRP8-NPM). Interestingly, hMRP8-NPMc+ transgenic mice developed myeloproliferation in bone marrow and spleen, whereas nontransgenic littermates and hMRP8-NPM transgenic mice remained disease free. These findings provide the first in vivo evidence indicating that NPMc+ confers a proliferative advantage in the myeloid lineage. No spontaneous acute myeloid leukemia was found in hMPR8-NPMc+ or hMRP8-NPM mice. This model will also aid in the development of therapeutic regimens that specifically target NPMc+.

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