about
Immunodeficiency and chronic myelogenous leukemia-like syndrome in mice with a targeted mutation of the ICSBP geneSelective regulatory function of Socs3 in the formation of IL-17-secreting T cellsGeneration of pathogenic T(H)17 cells in the absence of TGF-β signallingGenomic views of STAT function in CD4+ T helper cell differentiationOpposing regulation of the locus encoding IL-17 through direct, reciprocal actions of STAT3 and STAT5Lymphoid tissue inducer-like cells are an innate source of IL-17 and IL-22Tpl2 kinase regulates T cell interferon-gamma production and host resistance to Toxoplasma gondiiGlobal mapping of H3K4me3 and H3K27me3 reveals specificity and plasticity in lineage fate determination of differentiating CD4+ T cellsTranscription factors and CD4 T cells seeking identity: masters, minions, setters and spikersMechanisms underlying helper T-cell plasticity: implications for immune-mediated disease.Selective recognition of acetylated histones by bromodomain proteins visualized in living cellsA mouse model of HIES reveals pro- and anti-inflammatory functions of STAT3.The transcription factors Thpok and LRF are necessary and partly redundant for T helper cell differentiationProliferation conditions promote intrinsic changes in NK cells for an IL-10 response.Discrete roles of STAT4 and STAT6 transcription factors in tuning epigenetic modifications and transcription during T helper cell differentiation.Jak3-independent trafficking of the common gamma chain receptor subunit: chaperone function of Jaks revisited.Transcriptional and epigenetic control of T helper cell specification: molecular mechanisms underlying commitment and plasticity.Helper T cell diversity and plasticityGamma interferon triggers interaction between ICSBP (IRF-8) and TEL, recruiting the histone deacetylase HDAC3 to the interferon-responsive element.In search of magic bullets: the golden age of immunotherapeutics.Helper T cell plasticity: impact of extrinsic and intrinsic signals on transcriptomes and epigenomes.Super-enhancers delineate disease-associated regulatory nodes in T cells.Interaction of histone acetylases and deacetylases in vivo.Tissue inhibitor of metalloproteinase 1 is preferentially expressed in Th1 and Th17 T-helper cell subsets and is a direct STAT target gene.Transcriptional and epigenetic networks of helper T and innate lymphoid cells.Diverse targets of the transcription factor STAT3 contribute to T cell pathogenicity and homeostasis.Signal transduction pathways and transcriptional regulation in Th17 cell differentiationCytokine signaling: birth of a pathway.PAPST, a User Friendly and Powerful Java Platform for ChIP-Seq Peak Co-Localization Analysis and Beyond.Functional and epigenetic studies reveal multistep differentiation and plasticity of in vitro-generated and in vivo-derived follicular T helper cellsEZH2 is crucial for both differentiation of regulatory T cells and T effector cell expansion.Nonredundant roles for Stat5a/b in directly regulating Foxp3Proprotein convertase furin is preferentially expressed in T helper 1 cells and regulates interferon gamma.Interleukin-23-Induced Transcription Factor Blimp-1 Promotes Pathogenicity of T Helper 17 Cells.Mechanisms of Jak/STAT signaling in immunity and diseaseImmune cell-specific amplification of interferon signaling by the IRF-4/8-PU.1 complex.Regulating type 1 IFN effects in CD8 T cells during viral infections: changing STAT4 and STAT1 expression for functionRetinoic acid inhibits Th17 polarization and enhances FoxP3 expression through a Stat-3/Stat-5 independent signaling pathwaySTATs shape the active enhancer landscape of T cell populationsDistinct requirements for T-bet in gut innate lymphoid cells
P50
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P50
description
hulumtuese
@sq
researcher
@en
wetenschapper
@nl
հետազոտող
@hy
name
Yuka Kanno
@ast
Yuka Kanno
@en
Yuka Kanno
@es
Yuka Kanno
@nl
Yuka Kanno
@sl
type
label
Yuka Kanno
@ast
Yuka Kanno
@en
Yuka Kanno
@es
Yuka Kanno
@nl
Yuka Kanno
@sl
prefLabel
Yuka Kanno
@ast
Yuka Kanno
@en
Yuka Kanno
@es
Yuka Kanno
@nl
Yuka Kanno
@sl
P106
P1153
7102772141
P21
P31
P496
0000-0001-5668-9319