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Open AccessJournal ArticleDOI

Jak2 Is Essential for Signaling through a Variety of Cytokine Receptors

TLDR
Reconstitution experiments demonstrate that Jak2 is not required for the generation of lymphoid progenitors, their amplification, or functional differentiation, and plays a critical, nonredundant role in the function of a specific group of cytokines receptors.
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This article is published in Cell.The article was published on 1998-05-01 and is currently open access. It has received 1110 citations till now. The article focuses on the topics: Janus kinase 2 & Signal transduction.

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Interferon-γ: an overview of signals, mechanisms and functions

TL;DR: The current understanding of IFN‐γ ligand, receptor, ignal transduction, and cellular effects with a focus on macrophage responses and to a lesser extent, responses from other cell types that influence macrophages function during infection are reviewed.
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A Gain-of-Function Mutation of JAK2 in Myeloproliferative Disorders

TL;DR: Genetic evidence and in vitro functional studies indicate that V617F gives hematopoietic precursors proliferative and survival advantages and a high proportion of patients with myeloproliferative disorders carry a dominant gain-of-function mutation of JAK2.
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Antiviral Actions of Interferons

TL;DR: Tremendous progress has been made in understanding the molecular basis of the antiviral actions of interferons (IFNs), as well as strategies evolved by viruses to antagonize the actions of IFNs.
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Demonstration of an interferon γ-dependent tumor surveillance system in immunocompetent mice

TL;DR: It is demonstrated that endogenously produced interferon gamma (IFN-gamma) forms the basis of a tumor surveillance system that controls development of both chemically induced and spontaneously arising tumors in mice and is evidenced by the finding that certain types of human tumors become selectively unresponsive to IFN-Gamma.
References
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Journal ArticleDOI

AML1, the Target of Multiple Chromosomal Translocations in Human Leukemia, Is Essential for Normal Fetal Liver Hematopoiesis

TL;DR: The results suggest that AML1-regulated target genes are essential for definitive hematopoiesis of all lineages, and that this defect was intrinsic to the stem cells in that AMl1-/-ES cells failed to contribute to hematocerosis in chimeric animals.
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Requirement of transcription factor PU.1 in the development of multiple hematopoietic lineages

TL;DR: The developmental programs of lymphoid and myeloid lineages require a common genetic function likely acting at the level of a multipotential progenitor, and mice carrying a mutation in the PU.1 locus were generated by gene targeting.
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Lymphopenia in interleukin (IL)-7 gene-deleted mice identifies IL-7 as a nonredundant cytokine.

TL;DR: The IL-7-deficient mice are the first example of single cytokine- deficient mice that exhibit severe lymphoid abnormalities and data show that proper T and B cell development is dependent on IL- 7.
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An early haematopoietic defect in mice lacking the transcription factor GATA-2.

TL;DR: It is demonstrated that the transcription factor GATA-2 plays a critical role in haematopoiesis, particularly of an adult type, and proposed that it regulates genes controlling growth factor responsiveness or the proliferative capacity of early haem atopoietic cells.
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Erythroid differentiation in chimaeric mice blocked by a targeted mutation in the gene for transcription factor GATA-1

TL;DR: The disruption of the X-linked GATA-1 gene by homologous recombination in a male (XY) murine embryonic stem cell line and testing the Gata-1-deficient cells for their ability to contribute to different tissues in chimaeric mice demonstrates that GATA, the zinc-finger transcription factor, is required for the normal differentiation of erythroid cells, and that other GATAS cannot compensate for its absence.
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