Reduced PU.1 expression causes myeloid progenitor expansion and increased leukemia penetrance in mice expressing PML-RARalpha. - Wikidata - awgldk - TriplyDB

Reduced PU.1 expression causes myeloid progenitor expansion and increased leukemia penetrance in mice expressing PML-RARalpha.

Reduced PU.1 expression causes myeloid progenitor expansion and increased leukemia penetrance in mice expressing PML-RARalpha.

http://www.wikidata.org/entity/Q33920326

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Mouse models for radiation-induced cancers PU.1 downregulation in murine radiation-induced acute myeloid leukaemia (AML): from molecular mechanism to human AML Mouse models for efficacy testing of agents against radiation carcinogenesis—a literature review Knockdown of Hspa9, a del(5q31.2) gene, results in a decrease in hematopoietic progenitors in mice Identification of a myeloid committed progenitor as the cancer-initiating cell in acute promyelocytic leukemia.Radiation-induced myeloid leukemia in murine models.A protease-resistant PML-RAR{alpha} has increased leukemogenic potential in a murine model of acute promyelocytic leukemia The Runx-PU.1 pathway preserves normal and AML/ETO9a leukemic stem cells.MIR125B1 represses the degradation of the PML-RARA oncoprotein by an autophagy-lysosomal pathway in acute promyelocytic leukemia.Expression and function of PML-RARA in the hematopoietic progenitor cells of Ctsg-PML-RARA mice PML-RARA can increase hematopoietic self-renewal without causing a myeloproliferative disease in mice.Sequencing a mouse acute promyelocytic leukemia genome reveals genetic events relevant for disease progression NRH:quinone oxidoreductase 2-deficient mice are highly susceptible to radiation-induced B-cell lymphomas Sox4 cooperates with PU.1 haploinsufficiency in murine myeloid leukemia.Expression of a bcr-1 isoform of RARalpha-PML does not affect the penetrance of acute promyelocytic leukemia or the acquisition of an interstitial deletion on mouse chromosome 2 Rara haploinsufficiency modestly influences the phenotype of acute promyelocytic leukemia in mice.A distal single nucleotide polymorphism alters long-range regulation of the PU.1 gene in acute myeloid leukemia.PU.1 affects proliferation of the human acute myeloid leukemia U937 cell line by directly regulating MEIS1.PML-retinoic acid receptor alpha inhibits PML IV enhancement of PU.1-induced C/EBPepsilon expression in myeloid differentiation.JNK-dependent gene regulatory circuitry governs mesenchymal fate.The significance of low PU.1 expression in patients with acute promyelocytic leukemia.Genome-scale definition of the transcriptional programme associated with compromised PU.1 activity in acute myeloid leukaemia.Pharmacogenetics of alkylator-associated acute myeloid leukemia.Structurally differentiated cis-elements that interact with PU.1 are functionally distinguishable in acute promyelocytic leukemia.Quantitative trait loci associated with susceptibility to therapy-related acute murine promyelocytic leukemia in hCG-PML/RARA transgenic mice Analysis of concentration-dependent functions of PU.1 in hematopoiesis using mouse models.Rapid and reliable diagnosis of murine myeloid leukemia (ML) by FISH of peripheral blood smear using probe of PU. 1, a candidate ML tumor suppressor.Transcriptional dysregulation during myeloid transformation in AML.Disruption of NAD(P)H:quinone oxidoreductase 1 gene in mice leads to radiation-induced myeloproliferative disease.Candidate metastasis suppressor genes uncovered by array comparative genomic hybridization in a mouse allograft model of prostate cancer.Notch signaling in acute promyelocytic leukemia Positive feedback between PU.1 and the cell cycle controls myeloid differentiation The transcription factor PU.1 is a critical regulator of cellular communication in the immune system.Oncogenic K-ras cooperates with PML-RAR alpha to induce an acute promyelocytic leukemia-like disease.Commonly dysregulated genes in murine APL cells.Interferon regulatory factor-8 is indispensable for the expression of promyelocytic leukemia and the formation of nuclear bodies in myeloid cells.Senescence is a Spi1-induced anti-proliferative mechanism in primary hematopoietic cells.Distinct roles for SCL in erythroid specification and maturation in zebrafish.Haploinsufficiency for DNA methyltransferase 3A predisposes hematopoietic cells to myeloid malignancies.Pin1-mediated prolyl isomerization of Runx1 affects PU.1 expression in pre-monocytes.

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Reduced PU.1 expression causes myeloid progenitor expansion and increased leukemia penetrance in mice expressing PML-RARalpha.

http://www.wikidata.org/entity/Q33920326

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2005 nî lūn-bûn

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2005 թուականի Օգոստոսին հրատարակուած գիտական յօդուած

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2005 թվականի օգոստոսին հրատարակված գիտական հոդված

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2005年の論文

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2005年論文

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2005年論文

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2005年论文

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Reduced PU.1 expression causes ...... mice expressing PML-RARalpha.

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Proceedings of the National Academy of Sciences of the United States of America

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Reduced PU.1 expression causes ...... n mice expressing PML-RARalpha

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Elaine R Mardis

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John S Park

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Matthew J Walter

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Michael McLellan

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Rhonda E Ries

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Richard K Wilson

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Sara Jaeger

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Timothy J Ley

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P2860

Early myeloid cell-specific expression of the human cathepsin G gene in transgenic mice

WT-1 is required for early kidney development

BCL-2 cooperates with promyelocytic leukemia retinoic acid receptor alpha chimeric protein (PMLRARalpha) to block neutrophil differentiation and initiate acute leukemia.

Seed versus soil: the importance of the target cell for transgenic models of human leukemias.

Neutrophil elastase is important for PML-retinoic acid receptor alpha activities in early myeloid cells.

Advantages of the CBA mouse in leukemogenesis research.

A pilot study of high-throughput, sequence-based mutational profiling of primary human acute myeloid leukemia cell genomes.

Characterization of genetic instability in radiation- and benzene-induced murine acute leukemia.

HOXB6 overexpression in murine bone marrow immortalizes a myelomonocytic precursor in vitro and causes hematopoietic stem cell expansion and acute myeloid leukemia in vivo.

Targeted disruption of the PU.1 gene results in multiple hematopoietic abnormalities

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10.1073/PNAS.0504247102

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