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Transient LMO2 expression is sufficient for oncogenic function and induction of T-ALL. The resulting T-ALLs lacked LMO2 and its target-gene expression, and histologically, transcriptionally, and genetically similar to human LMO2-driven T-ALL.
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Trichostatin A (TSA, a HDAC inhibitor) addition significantly attenuates MTX unsensitivity caused by dysfunction of LMO2/ZEB1 signaling. In conclusion, these findings have identified a molecular mechanism underlying LMO2/ZEB1-mediated leukaemogenesis, paving a way for treating T-ALL with a new strategy of epigenetic inhibitors.
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Genome-wide analysis indicated that LMO2 is required at the hemangioblast stage to position the TAL1/LMO2/LDB1 complex to regulatory elements that are important for the establishment of the hematopoietic developmental program.
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DNM2 mutations cooperate with Lmo2 T-cell oncogenes by enhancing IL-7 signalling.
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Hhex regulates Kit to promote radioresistance of self-renewing thymocytes in Lmo2-transgenic mice.
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HHEX is a direct transcriptional target of LMO2 consistent with its concordant gene expression.
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GATA2 and Lmo2 cooperatively regulate VEGF-induced angiogenesis and lymphangiogenesis via NRP2.
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a regulatory hierarchy of HOX control of LMO2 in normal development
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Lyl1 is critical for all oncogenic functions of Lmo2, including upregulation of a stem cell-like gene signature, aberrant self-renewal of thymocytes, and subsequent generation of T-cell leukemia.
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A model in which the distal control region functions through a chromatin looping mechanism to contact and enhance Lmo2 transcription specifically in erythroid cells.
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Studied the solution structure of Lmo2(LIM2) /Ldb1(LID) complex. Results show modular binding of tandem LIM domains in Lmo2 to tandem linear motifs in Ldb1 is accompanied by several disorder-to-order transitions/ conformational changes in both proteins.
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Studies demonstrate that Etv2 is expressed during and required for yolk sac hematoendothelial development, and that Lmo2 is one of the downstream targets of Etv2.
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This result raises the possibility that oncogenic Lck may activate Lmo2 promoter through direct interaction.
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Data show that thymic expression of the Tal1 and Lmo2 oncogenes results in rapid development of T-ALL, and similar to T-ALL patients, more than half the leukemic mice develop spontaneous mutations in Notch1.
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Notch1 mutation and Arf inactivation appear to independently cooperate in no requisite order with Lmo2 overexpression in inducing T-ALL, and all 3 events remained insufficient to guarantee immediate tumor development.
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DNA-binding activity of Tal1 is not required to cooperate with Lmo2 to cause leukemia in mice
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The molecular basis of Lmo2-induced T-cell acute lymphoblastic leukemia.
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Results suggest that alterations in gene expression of Gata6, Tspan8, S100a8, and Lmo2 may act via novel pathways that play functionally important roles in Men1-associated tumor progression.
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findings show that Lmo2 promotes the self-renewal of preleukemic thymocytes, providing a mechanism by which committed T cells can then accumulate additional genetic mutations required for leukemic transformation
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there is no mandatory role for LMO2 in lymphoid development, implying that its specific role in T-cell tumorigenesis results from a reprogramming of gene expression after enforced expression in T-cell precursors
