Notch activation is an early and critical event during T-Cell leukemogenesis in Ikaros-deficient mice - Wikidata - wikimedia - TriplyDB

Notch activation is an early and critical event during T-Cell leukemogenesis in Ikaros-deficient mice

Notch activation is an early and critical event during T-Cell leukemogenesis in Ikaros-deficient mice

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Selective regulation of lymphopoiesis and leukemogenesis by individual zinc fingers of Ikaros Deletion of the RNA-binding proteins ZFP36L1 and ZFP36L2 leads to perturbed thymic development and T lymphoblastic leukemia Role of Ikaros in T-cell acute lymphoblastic leukemia TLR7/9 versus TLR3/MDA5 signaling during virus infections and diabetes The Ikaros family of zinc-finger proteins Congenital pancytopenia and absence of B lymphocytes in a neonate with a mutation in the Ikaros gene Rbm15 modulates Notch-induced transcriptional activation and affects myeloid differentiation Alpha-secretase inhibition reduces human glioblastoma stem cell growth in vitro and in vivo by inhibiting Notch.Speed of leukemia development and genetic diversity in xenograft models of T cell acute lymphoblastic leukemia.RelB-dependent stromal cells promote T-cell leukemogenesis Hes1 potentiates T cell lymphomagenesis by up-regulating a subset of notch target genes.Tumor suppressors BTG1 and IKZF1 cooperate during mouse leukemia development and increase relapse risk in B-cell precursor acute lymphoblastic leukemia patients.Mutant Ikzf1, KrasG12D, and Notch1 cooperate in T lineage leukemogenesis and modulate responses to targeted agents.Gene expression profiling of murine T-cell lymphoblastic lymphoma identifies deregulation of S-phase initiating genes.Targeting surface nucleolin with multivalent HB-19 and related Nucant pseudopeptides results in distinct inhibitory mechanisms depending on the malignant tumor cell type Enhanced Notch activation is advantageous but not essential for T cell lymphomagenesis in Id1 transgenic mice Notch target gene deregulation and maintenance of the leukemogenic phenotype do not require RBP-J kappa in Ikaros null mice.Notch signalling in T-cell lymphoblastic leukaemia/lymphoma and other haematological malignancies.Inhibition of Notch signaling by a γ-secretase inhibitor attenuates hepatic fibrosis in rats.Deletion-based mechanisms of Notch1 activation in T-ALL: key roles for RAG recombinase and a conserved internal translational start site in Notch1.Predominant interaction of both Ikaros and Helios with the NuRD complex in immature thymocytes.Two functional loci in the promoter of EPAS1 gene involved in high-altitude adaptation of Tibetans.Alternative promoter usage at the Notch1 locus supports ligand-independent signaling in T cell development and leukemogenesis.Inhibitory effects of transcription factor Ikaros on the expression of liver cancer stem cell marker CD133 in hepatocellular carcinoma.c-Myc is an important direct target of Notch1 in T-cell acute lymphoblastic leukemia/lymphoma.Oncogenic activation of the Notch1 gene by deletion of its promoter in Ikaros-deficient T-ALL.Regulator of myeloid differentiation and function: The secret life of Ikaros.Insertional mutagenesis and deep profiling reveals gene hierarchies and a Myc/p53-dependent bottleneck in lymphomagenesis.Ikaros-Notch axis in host hematopoietic cells regulates experimental graft-versus-host disease.Notch1 contributes to mouse T-cell leukemia by directly inducing the expression of c-myc Notch1 inhibition targets the leukemia-initiating cells in a Tal1/Lmo2 mouse model of T-ALL.Cell of origin strongly influences genetic selection in a mouse model of T-ALL Ikaros is required for plasmacytoid dendritic cell differentiation.Illegitimate V(D)J recombination involving nonantigen receptor loci in lymphoid malignancy.Regulation of gene expression dynamics during developmental transitions by the Ikaros transcription factor.GATA-1 utilizes Ikaros and polycomb repressive complex 2 to suppress Hes1 and to promote erythropoiesis The SCFFBW7 ubiquitin ligase complex as a tumor suppressor in T cell leukemia Ikaros mediates gene silencing in T cells through Polycomb repressive complex 2.Notch 1 activation in the molecular pathogenesis of T-cell acute lymphoblastic leukaemia.Function of Ikaros as a tumor suppressor in B cell acute lymphoblastic leukemia

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Notch activation is an early and critical event during T-Cell leukemogenesis in Ikaros-deficient mice

http://www.wikidata.org/entity/Q34233443

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2006 nî lūn-bûn

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Notch activation is an early a ...... nesis in Ikaros-deficient mice

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Notch activation is an early a ...... nesis in Ikaros-deficient mice

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Notch activation is an early a ...... nesis in Ikaros-deficient mice

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Notch activation is an early a ...... nesis in Ikaros-deficient mice

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MCB.26.1.209-220.2006

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Molecular and Cellular Biology

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Notch activation is an early a ...... nesis in Ikaros-deficient mice

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Alexis Dumortier

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Christelle Thibault

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Eva Kleinmann

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Jacques Ghysdael

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Jennifer A Punt

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MacLean Sellars

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Philippe Kastner

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P2860

Expression pattern of notch1, 2 and 3 and Jagged1 and 2 in lymphoid and stromal thymus components: distinct ligand-receptor interactions in intrathymic T cell development

TAN-1, the human homolog of the Drosophila notch gene, is broken by chromosomal translocations in T lymphoblastic neoplasms

Repression by Ikaros and Aiolos is mediated through histone deacetylase complexes

Expression of dominant-negative and mutant isoforms of the antileukemic transcription factor Ikaros in infant acute lymphoblastic leukemia

Zinc finger-mediated protein interactions modulate Ikaros activity, a molecular control of lymphocyte development

Cluster analysis and display of genome-wide expression patterns

Analysis of Relative Gene Expression Data Using Real-Time Quantitative PCR and the 2−ΔΔCT Method

Expression of aberrantly spliced oncogenic ikaros isoforms in childhood acute lymphoblastic leukemia

Ikaros DNA-binding proteins direct formation of chromatin remodeling complexes in lymphocytes

Ikaros interactions with CtBP reveal a repression mechanism that is independent of histone deacetylase activity

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10.1128/MCB.26.1.209-220.2006

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