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Raptorfl mice

Manufactured by Jackson ImmunoResearch
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The Raptorfl/+ mice are a genetically modified mouse line developed by Jackson ImmunoResearch. These mice express a fluorescent reporter gene, allowing for the visualization and tracking of specific cell populations in research applications.

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Lab products found in correlation

Wild type fvb n mice, by Jackson ImmunoResearch (1 mentions) Wild type fvb n mice, by Charles River Laboratories (1 mentions)

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Raptorfl/fl mice (8 citations)

2 protocols using raptorfl mice

1

Generating Hepatoblastoma Mouse Model

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Wild-type FVB/N mice were obtained from Jackson Laboratory (Bar Harbor, ME). Raptorfl/+ mice [32 (link)] were purchased from the Jackson Laboratory (Bar Harbor, ME, USA; stock: 013188) and intercrossed to generate Raptorfl/fl mice. SB-mediated hydrodynamic injections were performed as described [33 (link)]. Briefly, for the HB tumorigenesis model, 20 μg of pT3-EF1α-YAPS127A and 20 μg of pT3-EF1αH-ΔN90-β-catenin along with SB transposase in a ratio of 25:1 were delivered into the FVB/N mouse by hydrodynamic injection. These two plasmids contain constitutively active forms of YAP and β-catenin protooncogenes. For further knocking out Raptor in the HB model, either 40μg pT3-EF1a or 40μg pT3-EF1a-Cre were co-injected with 20μg pT3-EF1α-YAPS127A and 20μg pT3-EF1α-ΔN90-beta-catenin together as well as 3.2μg pCMV-SB in Raptorfl/fl mice. All mice were monitored closely and euthanized as described in the main text. Mice were fed and monitored according to protocols approved by the Committee for Animal Research at the University of California, San Francisco.
Liu P., Calvisi D.F., Kiss A., Cigliano A., Schaff Z., Che L., Ribback S., Dombrowski F., Zhao D, & Chen X. (2017). Central role of mTORC1 downstream of YAP/TAZ in hepatoblastoma development. Oncotarget, 8(43), 73433-73447.
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2

Genetic Mouse Models for Liver Cancer

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Wild-type FVB/N mice were obtained from Charles River (Wilmington, MA). AKT2 knockout mice [16 (link)] were generated by crossing AKT2+/− mice. Raptorfl/+ mice [17 (link)] were purchased from the Jackson Laboratory (Bar Harbor, ME; stock: 013188), and intercrossed to generate Raptorfl/fl mice. Hydrodynamic injections were performed as described [18 (link)]. To determine whether overexpression of PIK3CA plasmid alone can induce hepatic steatosis and carcinogenesis, 20μg PIK3CA WT, H1047R or E545K along with 0.8μg SB plasmid were delivered into FVB/N mouse liver by hydrodynamic injection. For the tumorigenesis models, 20μg H1047R or E545K, 20μg NRasV12 or c-Met along with 1.6μg SB plasmid were delivered into FVB/N mouse liver. The same amount and combination of plasmids were delivered into AKT2 wild-type and AKT2 knockout mice. To determine the requirement of mTORC1 in PIK3CA-dependent hepatocarcinogenesis, high dose of Cre (60μg) or pT3EF1α (60μg) was mixed with H1047R (20μg), c-Met (20μg) and SB (4μg), and injected into Raptorfl/fl mice. Mice were housed, fed, and monitored in accordance with protocols approved by the Committee for Animal Research at the University of California, San Francisco.
Wang C., Che L., Hu J., Zhang S., Jiang L., Latte G., Demartis M.I., Tao J., Gui B., Pilo M.G., Ribback S., Dombrowski F., Evert M., Calvisi D.F, & Chen X. (2016). Activated mutant forms of PIK3CA cooperate with RasV12 or c-Met to induce liver tumor formation in mice via AKT2/mTORC1 cascade. Liver international : official journal of the International Association for the Study of the Liver, 36(8), 1176-1186.
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