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注意:仅列出部分参考文献,下载原文获取全部文献信息。The miR-17-92 MicroRNA Cluster Is Regulated by Multiple Mechanisms in B-Cell Malignancies
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Subcellular Localization of Glycogen Synthase Kinase 3β Controls Embryonic Stem Cell Self-Renewal
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Dicer ablation affects antibody diversity and cell survival in the B lymphocyte lineage
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Targeted deletion reveals essential and overlapping functions of the miR-17∼92 family of miRNA clusters
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Antagomir-17-5p Abolishes the Growth of Therapy-Resistant Neuroblastoma through p21 and BIM
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Molecular subtypes of diffuse large B-cell lymphoma arise by distinct genetic pathways
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Transgenic over-expression of the microRNA miR-17-92 cluster promotes proliferation and inhibits differentiation of lung epithelial progenitor cells
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Augmentation of tumor angiogenesis by a Myc-activated microRNA cluster
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A polycistronic microRNA cluster, miR-17-92, is overexpressed in human lung cancers and enhances cell proliferation
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Gene expression profiling of mantle cell lymphoma cells reveals aberrant expression of genes from the PI3K-AKT, WNT and TGFβ signalling pathways
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Differential targeting of prosurvival Bcl-2 proteins by their BH3-only ligands allows complementary apoptotic function
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Bim is a suppressor of Myc-induced mouse B cell leukemia
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Optimal B-cell proliferation requires phosphoinositide 3-kinase-dependent inactivation of FOXO transcription factors
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Identification and characterization of a novel gene, C13orf25, as a target for 13q31-q32 amplification in malignant lymphoma
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Prediction of mammalian microRNA targets
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The proliferation gene expression signature is a quantitative integrator of oncogenic events that predicts survival in mantle cell lymphoma
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