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ADAR1 Knockout Inhibits Notch1-induced T-ALL in Mice / 中国实验血液学杂志
Journal of Experimental Hematology ; (6): 643-648, 2016.
Artigo em Chinês | WPRIM | ID: wpr-360032
ABSTRACT
<p><b>OBJECTIVE</b>To investigate the effect of ADAR1 on the occurrence and development of mouse T cell acute lymphoblastic leukemia (T-ALL).</p><p><b>METHODS</b>Lck-Cre; ADAR1lox/lox mice were generated through interbreeding. The lineage-cells of Lck-Cre; ADAR1lox/lox mice and the control were enriched respectively by the means of MACS, and the lin- cells were transfected with retrovirus carrying MSCV-ICN1-IRES-GFP fusion gene. Then the transfection efficiency was detected by the means of FACS, and the same number of GFP+ cells were transplanted into lethally irradiated recipient mice to observe the survival of mice in 2 recipient group after transplantation.</p><p><b>RESULTS</b>T cell-specific knockout ADAR1 mice were generated, and Notch1-induced T-ALL mouse model was established successfully. The leukemia with T-ALL characteristics occured in the mice of control group, but did not in the ADAR1 kmockout mice after transplantation.</p><p><b>CONCLUSIONS</b>ADAR1 plays a key role in the incidence and development of Notch1-induced T-ALL.</p>
Assuntos
Texto completo: DisponíveL Índice: WPRIM (Pacífico Ocidental) Assunto principal: Linfócitos T / Adenosina Desaminase / Camundongos Knockout / Modelos Animais de Doenças / Receptor Notch1 / Leucemia-Linfoma Linfoblástico de Células T Precursoras / Genética Tipo de estudo: Estudo prognóstico Limite: Animais Idioma: Chinês Revista: Journal of Experimental Hematology Ano de publicação: 2016 Tipo de documento: Artigo

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Texto completo: DisponíveL Índice: WPRIM (Pacífico Ocidental) Assunto principal: Linfócitos T / Adenosina Desaminase / Camundongos Knockout / Modelos Animais de Doenças / Receptor Notch1 / Leucemia-Linfoma Linfoblástico de Células T Precursoras / Genética Tipo de estudo: Estudo prognóstico Limite: Animais Idioma: Chinês Revista: Journal of Experimental Hematology Ano de publicação: 2016 Tipo de documento: Artigo