about
STAT4 requires the N-terminal domain for efficient phosphorylationSTAT4: a critical regulator of inflammation in vivoSTAT6-mediated keratitis and blepharitis: a novel murine model of ocular atopic dermatitisThe transcription factor PU.1 regulates γδ T cell homeostasisThe transcription factor Etv5 controls TH17 cell development and allergic airway inflammation.The transcription factor PU.1 is required for the development of IL-9-producing T cells and allergic inflammation.The signal transducer and activator of transcription 6 gene (STAT6) increases the propensity of patients with atopic dermatitis toward disseminated viral skin infections.Increased skin barrier disruption by sodium lauryl sulfate in mice expressing a constitutively active STAT6 in T cells.Stat6-deficient mice develop airway hyperresponsiveness and peribronchial fibrosis during chronic fungal asthma.TH9 cells are required for tissue mast cell accumulation during allergic inflammationAltered STAT4 Isoform Expression in Patients with Inflammatory Bowel Disease.Gcn5 is required for PU.1-dependent IL-9 induction in Th9 cells.STAT4 deficiency reduces the development of atherosclerosis in mice.Diverse inflammatory cytokines induce selectin ligand expression on murine CD4 T cells via p38α MAPK.Scratching the surface: towards understanding the pathogenesis of atopic dermatitis.The transcription factor Twist1 limits T helper 17 and T follicular helper cell development by repressing the gene encoding the interleukin-6 receptor α chain.Impaired development of human Th1 cells in patients with deficient expression of STAT4.Th9 cell development requires a BATF-regulated transcriptional networkSTAT4 is critical for immunity but not for antileishmanial activity of antimonials in experimental visceral leishmaniasis.Th9 cells: differentiation and disease.Transcriptional regulation by STAT6.The symphony of the ninth: the development and function of Th9 cells.Mast Cells Regulate Epidermal Barrier Function and the Development of Allergic Skin Inflammation.PARP14 limits severity of allergic skin disease.Paracrine IL-2 Is Required for Optimal Type 2 Effector Cytokine Production.The ETS Family Transcription Factors Etv5 and PU.1 Function in Parallel To Promote Th9 Cell DevelopmentCD4+ T-cell-mediated anti-tumor immunity can be uncoupled from autoimmunity via the STAT4/STAT6 signaling axis.STAT3 Impairs STAT5 Activation in the Development of IL-9-Secreting T CellsDifferential requirement of signal transducer and activator of transcription-4 (Stat4) and Stat6 in a thyrotropin receptor-289-adenovirus-induced model of Graves' hyperthyroidism.STAT4 is required for IL-23 responsiveness in Th17 memory cells and NKT cells.PU.1 Expression in T Follicular Helper Cells Limits CD40L-Dependent Germinal Center B Cell DevelopmentAn Inhibitory Role for the Transcription Factor Stat3 in Controlling IL-4 and Bcl6 Expression in Follicular Helper T Cells.Impaired IL-12 responses and enhanced development of Th2 cells in Stat4-deficient mice.The TNF-family ligand TL1A and its receptor DR3 promote T cell-mediated allergic immunopathology by enhancing differentiation and pathogenicity of IL-9-producing T cells.STAT3 Activation Impairs the Stability of Th9 CellsTwist1 regulates Ifng expression in Th1 cells by interfering with Runx3 function.Stat4 limits DNA methyltransferase recruitment and DNA methylation of the IL-18Ralpha gene during Th1 differentiation.Yoking OX40 to regulation of IL-9.Elevated IL-6 expression in CD4 T cells via PKCtheta and NF-kappaB induces Th2 cytokine production.Topical application of a vitamin D analogue exacerbates atopic dermatitis and induces the atopic dermatitis-like phenotype in Stat6VT mice.
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description
hulumtues
@sq
researcher
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ricercatore
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wetenschapper
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հետազոտող
@hy
name
Mark H. Kaplan
@en
Mark H. Kaplan
@es
Mark H. Kaplan
@nl
Mark H. Kaplan
@sl
Mark Kaplan
@de
type
label
Mark H. Kaplan
@en
Mark H. Kaplan
@es
Mark H. Kaplan
@nl
Mark H. Kaplan
@sl
Mark Kaplan
@de
prefLabel
Mark H. Kaplan
@en
Mark H. Kaplan
@es
Mark H. Kaplan
@nl
Mark H. Kaplan
@sl
Mark Kaplan
@de
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0000 0001 1006 9341
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0000-0002-2923-8245
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1951-01-01T00:00:00Z
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lccn-n95023535