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  1. AU="Emery H Bresnick"
  2. AU="McManus, R J"
  3. AU="Mahmoudi, Hamid Reza"
  4. AU="Lee, Dongil"
  5. AU="T Oni"
  6. AU="Diego R. Pérez-Salicrup"
  7. AU="Verhaaren, Benjamin F J"
  8. AU="Gamoudi, Gamoudi Amor"
  9. AU="Fonseca, Barbara F."
  10. AU="Rubio García, Rafael"
  11. AU="Jiménez-Solano, A"
  12. AU=Mai Huynh Kim
  13. AU=Ellis R J
  14. AU="Carvalho, Aline Carla Araújo"
  15. AU=Gleeson Sarah
  16. AU="Lozier, Alan P."
  17. AU="Perrin, Elodie"
  18. AU="Chung, Haniee"
  19. AU="Jendernalik, Kamila"
  20. AU="Naveira, Horacio F"
  21. AU="Heyliger, Jamie"
  22. AU="García-Fernández, Ciara"
  23. AU="Lee, Mi-Ock"
  24. AU="Pouraliakbar, Hamidreza"
  25. AU="Raina, Hema"
  26. AU="Rosenbaum, David P"
  27. AU="Paulus, Markus"
  28. AU="Nguyen, David Truong"
  29. AU="Khazanchi, Rakesh Kumar"
  30. AU="Agrò, Felice E"
  31. AU="Bücker, Bettina"
  32. AU="Steussy, Bryan W"

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Treffer 1 - 10 von insgesamt 17

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  1. Artikel ; Online: Restricting genomic actions of innate immune mediators on fetal hematopoietic progenitor cells

    Vu L. Tran / Peng Liu / Koichi R. Katsumura / Erin Kim / Bjorn M. Schoff / Kirby D. Johnson / Emery H. Bresnick

    iScience, Vol 26, Iss 4, Pp 106297- (2023)

    2023  

    Abstract: Summary: Innate immune signaling protects against pathogens, controls hematopoietic development, and functions in oncogenesis, yet the relationship between these mechanisms is undefined. Downregulating the GATA2 transcription factor in fetal ... ...

    Abstract Summary: Innate immune signaling protects against pathogens, controls hematopoietic development, and functions in oncogenesis, yet the relationship between these mechanisms is undefined. Downregulating the GATA2 transcription factor in fetal hematopoietic progenitor cells upregulates genes encoding innate immune regulators, increases Interferon-γ (IFNγ) signaling, and disrupts differentiation. We demonstrate that deletion of an enhancer that confers GATA2 expression in fetal progenitors elevated Toll-like receptor (TLR) TLR1/2 and TLR2/6 expression and signaling. Rescue by expressing GATA2 downregulated elevated TLR signaling. IFNγ amplified TLR1/2 and TLR2/6 signaling in GATA2-deficient progenitors, synergistically activating cytokine/chemokine genes and elevating cytokine/chemokine production in myeloid cell progeny. Genomic analysis of how innate immune signaling remodels the GATA2-deficient progenitor transcriptome revealed hypersensitive responses at innate immune genes harboring motifs for signal-dependent transcription factors and factors not linked to these mechanisms. As GATA2 establishes a transcriptome that constrains innate immune signaling, insufficient GATA2 renders fetal progenitor cells hypersensitive to innate immune signaling.
    Schlagwörter Molecular mechanism of gene regulation ; Immunology ; Transcriptomics ; Science ; Q
    Sprache Englisch
    Erscheinungsdatum 2023-04-01T00:00:00Z
    Verlag Elsevier
    Dokumenttyp Artikel ; Online
    Datenquelle BASE - Bielefeld Academic Search Engine (Lebenswissenschaftliche Auswahl)

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  2. Artikel ; Online: A transcriptional network governing ceramide homeostasis establishes a cytokine-dependent developmental process

    Ruiqi Liao / Abiola Babatunde / Stephanie Qiu / Hamsini Harikumar / Joshua J. Coon / Katherine A. Overmyer / Yusuf A. Hannun / Chiara Luberto / Emery H. Bresnick

    Nature Communications, Vol 14, Iss 1, Pp 1-

    2023  Band 16

    Abstract: Abstract Transcriptional mechanisms controlling developmental processes establish and maintain proteomic networks, which can govern the levels of intracellular small molecules. Although dynamic changes in bioactive small molecules can link transcription ... ...

    Abstract Abstract Transcriptional mechanisms controlling developmental processes establish and maintain proteomic networks, which can govern the levels of intracellular small molecules. Although dynamic changes in bioactive small molecules can link transcription factor and genome activity with cell state transitions, many mechanistic questions are unresolved. Using quantitative lipidomics and multiomics, we discover that the hematopoietic transcription factor GATA1 establishes ceramide homeostasis during erythroid differentiation by regulating genes encoding sphingolipid metabolic enzymes. Inhibiting a GATA1-induced sphingolipid biosynthetic enzyme, delta(4)-desaturase, or disrupting ceramide homeostasis with cell-permeable dihydroceramide or ceramide is detrimental to erythroid, but not myeloid, progenitor activity. Coupled with genetic editing-based rewiring of the regulatory circuitry, we demonstrate that ceramide homeostasis commissions vital stem cell factor and erythropoietin signaling by opposing an inhibitory protein phosphatase 2A-dependent, dual-component mechanism. Integrating bioactive lipids as essential components of GATA factor mechanisms to control cell state transitions has implications for diverse cell and tissue types.
    Schlagwörter Science ; Q
    Thema/Rubrik (Code) 570
    Sprache Englisch
    Erscheinungsdatum 2023-11-01T00:00:00Z
    Verlag Nature Portfolio
    Dokumenttyp Artikel ; Online
    Datenquelle BASE - Bielefeld Academic Search Engine (Lebenswissenschaftliche Auswahl)

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  3. Artikel ; Online: Pathogenic human variant that dislocates GATA2 zinc fingers disrupts hematopoietic gene expression and signaling networks

    Mabel Minji Jung / Siqi Shen / Giovanni A. Botten / Thomas Olender / Koichi R. Katsumura / Kirby D. Johnson / Alexandra A. Soukup / Peng Liu / Qingzhou Zhang / Zena D. Jensvold / Peter W. Lewis / Robert A. Beagrie / Jason K.K. Low / Lihua Yang / Joel P. Mackay / Lucy A. Godley / Marjorie Brand / Jian Xu / Sunduz Keles /
    Emery H. Bresnick

    The Journal of Clinical Investigation, Vol 133, Iss

    2023  Band 7

    Abstract: Although certain human genetic variants are conspicuously loss of function, decoding the impact of many variants is challenging. Previously, we described a patient with leukemia predisposition syndrome (GATA2 deficiency) with a germline GATA2 variant ... ...

    Abstract Although certain human genetic variants are conspicuously loss of function, decoding the impact of many variants is challenging. Previously, we described a patient with leukemia predisposition syndrome (GATA2 deficiency) with a germline GATA2 variant that inserts 9 amino acids between the 2 zinc fingers (9aa-Ins). Here, we conducted mechanistic analyses using genomic technologies and a genetic rescue system with Gata2 enhancer–mutant hematopoietic progenitor cells to compare how GATA2 and 9aa-Ins function genome-wide. Despite nuclear localization, 9aa-Ins was severely defective in occupying and remodeling chromatin and regulating transcription. Variation of the inter–zinc finger spacer length revealed that insertions were more deleterious to activation than repression. GATA2 deficiency generated a lineage-diverting gene expression program and a hematopoiesis-disrupting signaling network in progenitors with reduced granulocyte-macrophage colony-stimulating factor (GM-CSF) and elevated IL-6 signaling. As insufficient GM-CSF signaling caused pulmonary alveolar proteinosis and excessive IL-6 signaling promoted bone marrow failure and GATA2 deficiency patient phenotypes, these results provide insight into mechanisms underlying GATA2-linked pathologies.
    Schlagwörter Genetics ; Hematology ; Medicine ; R
    Thema/Rubrik (Code) 572
    Sprache Englisch
    Erscheinungsdatum 2023-04-01T00:00:00Z
    Verlag American Society for Clinical Investigation
    Dokumenttyp Artikel ; Online
    Datenquelle BASE - Bielefeld Academic Search Engine (Lebenswissenschaftliche Auswahl)

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  4. Artikel ; Online: Discovering How Heme Controls Genome Function Through Heme-omics

    Ruiqi Liao / Ye Zheng / Xin Liu / Yuannyu Zhang / Gretchen Seim / Nobuyuki Tanimura / Gary M. Wilson / Peiman Hematti / Joshua J. Coon / Jing Fan / Jian Xu / Sunduz Keles / Emery H. Bresnick

    Cell Reports, Vol 31, Iss 13, Pp 107832- (2020)

    2020  

    Abstract: Summary: Protein ensembles control genome function by establishing, maintaining, and deconstructing cell-type-specific chromosomal landscapes. A plethora of small molecules orchestrate cellular functions and therefore may link physiological processes ... ...

    Abstract Summary: Protein ensembles control genome function by establishing, maintaining, and deconstructing cell-type-specific chromosomal landscapes. A plethora of small molecules orchestrate cellular functions and therefore may link physiological processes with genome biology. The metabolic enzyme and hemoglobin cofactor heme induces proteolysis of a transcriptional repressor, Bach1, and regulates gene expression post-transcriptionally. However, whether heme controls genome function broadly or through prescriptive actions is unclear. Using assay for transposase-accessible chromatin sequencing (ATAC-seq), we establish a heme-dependent chromatin atlas in wild-type and mutant erythroblasts lacking enhancers that confer normal heme synthesis. Amalgamating chromatin landscapes and transcriptomes in cells with sub-physiological heme and post-heme rescue reveals parallel Bach1-dependent and Bach1-independent mechanisms that target heme-sensing chromosomal hotspots. The hotspots harbor a DNA motif demarcating heme-regulated chromatin and genes encoding proteins not known to be heme regulated, including metabolic enzymes. The heme-omics analysis establishes how an essential biochemical cofactor controls genome function and cellular physiology.
    Schlagwörter heme ; erythroid ; erythroblast ; GATA1 ; Bach1 ; chromatin ; Biology (General) ; QH301-705.5
    Sprache Englisch
    Erscheinungsdatum 2020-06-01T00:00:00Z
    Verlag Elsevier
    Dokumenttyp Artikel ; Online
    Datenquelle BASE - Bielefeld Academic Search Engine (Lebenswissenschaftliche Auswahl)

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  5. Artikel ; Online: GATA Factor-Dependent Positive-Feedback Circuit in Acute Myeloid Leukemia Cells

    Koichi R. Katsumura / Irene M. Ong / Andrew W. DeVilbiss / Rajendran Sanalkumar / Emery H. Bresnick

    Cell Reports, Vol 16, Iss 9, Pp 2428-

    2016  Band 2441

    Abstract: The master regulatory transcription factor GATA-2 triggers hematopoietic stem and progenitor cell generation. GATA2 haploinsufficiency is implicated in myelodysplastic syndrome (MDS) and acute myeloid leukemia (AML), and GATA2 overexpression portends a ... ...

    Abstract The master regulatory transcription factor GATA-2 triggers hematopoietic stem and progenitor cell generation. GATA2 haploinsufficiency is implicated in myelodysplastic syndrome (MDS) and acute myeloid leukemia (AML), and GATA2 overexpression portends a poor prognosis for AML. However, the constituents of the GATA-2-dependent genetic network mediating pathogenesis are unknown. We described a p38-dependent mechanism that phosphorylates GATA-2 and increases GATA-2 target gene activation. We demonstrate that this mechanism establishes a growth-promoting chemokine/cytokine circuit in AML cells. p38/ERK-dependent GATA-2 phosphorylation facilitated positive autoregulation of GATA2 transcription and expression of target genes, including IL1B and CXCL2. IL-1β and CXCL2 enhanced GATA-2 phosphorylation, which increased GATA-2-mediated transcriptional activation. p38/ERK-GATA-2 stimulated AML cell proliferation via CXCL2 induction. As GATA2 mRNA correlated with IL1B and CXCL2 mRNAs in AML-M5 and high expression of these genes predicted poor prognosis of cytogenetically normal AML, we propose that the circuit is functionally important in specific AML contexts.
    Schlagwörter Biology (General) ; QH301-705.5
    Thema/Rubrik (Code) 570
    Sprache Englisch
    Erscheinungsdatum 2016-08-01T00:00:00Z
    Verlag Elsevier
    Dokumenttyp Artikel ; Online
    Datenquelle BASE - Bielefeld Academic Search Engine (Lebenswissenschaftliche Auswahl)

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  6. Artikel ; Online: Exosome complex orchestrates developmental signaling to balance proliferation and differentiation during erythropoiesis

    Skye C McIver / Koichi R Katsumura / Elsa Davids / Peng Liu / Yoon-A Kang / David Yang / Emery H Bresnick

    eLife, Vol

    2016  Band 5

    Abstract: Since the highly conserved exosome complex mediates the degradation and processing of multiple classes of RNAs, it almost certainly controls diverse biological processes. How this post-transcriptional RNA-regulatory machine impacts cell fate decisions ... ...

    Abstract Since the highly conserved exosome complex mediates the degradation and processing of multiple classes of RNAs, it almost certainly controls diverse biological processes. How this post-transcriptional RNA-regulatory machine impacts cell fate decisions and differentiation is poorly understood. Previously, we demonstrated that exosome complex subunits confer an erythroid maturation barricade, and the erythroid transcription factor GATA-1 dismantles the barricade by transcriptionally repressing the cognate genes. While dissecting requirements for the maturation barricade in Mus musculus, we discovered that the exosome complex is a vital determinant of a developmental signaling transition that dictates proliferation/amplification versus differentiation. Exosome complex integrity in erythroid precursor cells ensures Kit receptor tyrosine kinase expression and stem cell factor/Kit signaling, while preventing responsiveness to erythropoietin-instigated signals that promote differentiation. Functioning as a gatekeeper of this developmental signaling transition, the exosome complex controls the massive production of erythroid cells that ensures organismal survival in homeostatic and stress contexts.
    Schlagwörter erythroid ; progenitor ; signaling ; transcription ; Medicine ; R ; Science ; Q ; Biology (General) ; QH301-705.5
    Sprache Englisch
    Erscheinungsdatum 2016-08-01T00:00:00Z
    Verlag eLife Sciences Publications Ltd
    Dokumenttyp Artikel ; Online
    Datenquelle BASE - Bielefeld Academic Search Engine (Lebenswissenschaftliche Auswahl)

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  7. Artikel ; Online: GATA Factor-G-Protein-Coupled Receptor Circuit Suppresses Hematopoiesis

    Xin Gao / Tongyu Wu / Kirby D. Johnson / Jamie L. Lahvic / Erik A. Ranheim / Leonard I. Zon / Emery H. Bresnick

    Stem Cell Reports, Vol 6, Iss 3, Pp 368-

    2016  Band 382

    Abstract: Hematopoietic stem cells (HSCs) originate from hemogenic endothelium within the aorta-gonad-mesonephros (AGM) region of the mammalian embryo. The relationship between genetic circuits controlling stem cell genesis and multi-potency is not understood. A ... ...

    Abstract Hematopoietic stem cells (HSCs) originate from hemogenic endothelium within the aorta-gonad-mesonephros (AGM) region of the mammalian embryo. The relationship between genetic circuits controlling stem cell genesis and multi-potency is not understood. A Gata2 cis element (+9.5) enhances Gata2 expression in the AGM and induces the endothelial to HSC transition. We demonstrated that GATA-2 rescued hematopoiesis in +9.5−/− AGMs. As G-protein-coupled receptors (GPCRs) are the most common targets for FDA-approved drugs, we analyzed the GPCR gene ensemble to identify GATA-2-regulated GPCRs. Of the 20 GATA-2-activated GPCR genes, four were GATA-1-activated, and only Gpr65 expression resembled Gata2. Contrasting with the paradigm in which GATA-2-activated genes promote hematopoietic stem and progenitor cell genesis/function, our mouse and zebrafish studies indicated that GPR65 suppressed hematopoiesis. GPR65 established repressive chromatin at the +9.5 site, restricted occupancy by the activator Scl/TAL1, and repressed Gata2 transcription. Thus, a Gata2 cis element creates a GATA-2-GPCR circuit that limits positive regulators that promote hematopoiesis.
    Schlagwörter Medicine (General) ; R5-920 ; Biology (General) ; QH301-705.5
    Thema/Rubrik (Code) 570
    Sprache Englisch
    Erscheinungsdatum 2016-03-01T00:00:00Z
    Verlag Elsevier
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    Datenquelle BASE - Bielefeld Academic Search Engine (Lebenswissenschaftliche Auswahl)

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  8. Artikel ; Online: Polycomb Group Protein YY1 Is an Essential Regulator of Hematopoietic Stem Cell Quiescence

    Zhanping Lu / Courtney C. Hong / Guangyao Kong / Anna L.F.V. Assumpção / Irene M. Ong / Emery H. Bresnick / Jing Zhang / Xuan Pan

    Cell Reports, Vol 22, Iss 6, Pp 1545-

    2018  Band 1559

    Abstract: Summary: Yin yang 1 (YY1) is a ubiquitous transcription factor and mammalian polycomb group protein (PcG) with important functions to regulate embryonic development, lineage differentiation, and cell proliferation. YY1 mediates stable PcG-dependent ... ...

    Abstract Summary: Yin yang 1 (YY1) is a ubiquitous transcription factor and mammalian polycomb group protein (PcG) with important functions to regulate embryonic development, lineage differentiation, and cell proliferation. YY1 mediates stable PcG-dependent transcriptional repression via recruitment of PcG proteins that catalyze histone modifications. Many questions remain unanswered regarding how cell- and tissue-specificity is achieved by PcG proteins. Here, we demonstrate that a conditional knockout of Yy1 in hematopoietic stem cells (HSCs) decreases long-term repopulating activity and ectopic YY1 expression expands HSCs. Although the YY1 PcG domain is required for Igκ chain rearrangement in B cells, the YY1 mutant lacking the PcG domain retained the capacity to stimulate HSC self-renewal. YY1 deficiency deregulated the genetic network governing HSC cell proliferation and impaired stem cell factor/c-Kit signaling, disrupting mechanisms conferring HSC quiescence. These results reveal a mechanism for how a ubiquitously expressed transcriptional repressor mediates lineage-specific functions to control adult hematopoiesis.
    Schlagwörter YY1 ; polycomb group protein ; hematopoietic stem cell ; cell cycle ; quiescence ; c-Kit ; Biology (General) ; QH301-705.5
    Thema/Rubrik (Code) 571
    Sprache Englisch
    Erscheinungsdatum 2018-02-01T00:00:00Z
    Verlag Elsevier
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  9. Artikel ; Online: Integrating Enhancer Mechanisms to Establish a Hierarchical Blood Development Program

    Charu Mehta / Kirby D. Johnson / Xin Gao / Irene M. Ong / Koichi R. Katsumura / Skye C. McIver / Erik A. Ranheim / Emery H. Bresnick

    Cell Reports, Vol 20, Iss 12, Pp 2966-

    2017  Band 2979

    Abstract: Hematopoietic development requires the transcription factor GATA-2, and GATA-2 mutations cause diverse pathologies, including leukemia. GATA-2-regulated enhancers increase Gata2 expression in hematopoietic stem/progenitor cells and control hematopoiesis. ...

    Abstract Hematopoietic development requires the transcription factor GATA-2, and GATA-2 mutations cause diverse pathologies, including leukemia. GATA-2-regulated enhancers increase Gata2 expression in hematopoietic stem/progenitor cells and control hematopoiesis. The +9.5-kb enhancer activates transcription in endothelium and hematopoietic stem cells (HSCs), and its deletion abrogates HSC generation. The −77-kb enhancer activates transcription in myeloid progenitors, and its deletion impairs differentiation. Since +9.5−/− embryos are HSC deficient, it was unclear whether the +9.5 functions in progenitors or if GATA-2 expression in progenitors solely requires −77. We further dissected the mechanisms using −77;+9.5 compound heterozygous (CH) mice. The embryonic lethal CH mutation depleted megakaryocyte-erythrocyte progenitors (MEPs). While the +9.5 suffices for HSC generation, the −77 and +9.5 must reside on one allele to induce MEPs. The −77 generated burst-forming unit-erythroid through the induction of GATA-1 and other GATA-2 targets. The enhancer circuits controlled signaling pathways that orchestrate a GATA factor-dependent blood development program.
    Schlagwörter GATA-2 ; enhancer ; hematopoiesis ; erythroid ; myeloid ; progenitor ; mouse model ; Biology (General) ; QH301-705.5
    Thema/Rubrik (Code) 570
    Sprache Englisch
    Erscheinungsdatum 2017-09-01T00:00:00Z
    Verlag Elsevier
    Dokumenttyp Artikel ; Online
    Datenquelle BASE - Bielefeld Academic Search Engine (Lebenswissenschaftliche Auswahl)

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  10. Artikel ; Online: Long non-coding RNA-dependent mechanism to regulate heme biosynthesis and erythrocyte development

    Jinhua Liu / Yapu Li / Jingyuan Tong / Jie Gao / Qing Guo / Lingling Zhang / Bingrui Wang / Hui Zhao / Hongtao Wang / Erlie Jiang / Ryo Kurita / Yukio Nakamura / Osamu Tanabe / James Douglas Engel / Emery H. Bresnick / Jiaxi Zhou / Lihong Shi

    Nature Communications, Vol 9, Iss 1, Pp 1-

    2018  Band 15

    Abstract: LncRNAs modulate diverse physiological cellular processes, however, their involvement in heme-dependent processes are not yet clear. Here the authors reveal the role of lncRNA UCA1 in erythroid cell development. ...

    Abstract LncRNAs modulate diverse physiological cellular processes, however, their involvement in heme-dependent processes are not yet clear. Here the authors reveal the role of lncRNA UCA1 in erythroid cell development.
    Schlagwörter Science ; Q
    Sprache Englisch
    Erscheinungsdatum 2018-10-01T00:00:00Z
    Verlag Nature Publishing Group
    Dokumenttyp Artikel ; Online
    Datenquelle BASE - Bielefeld Academic Search Engine (Lebenswissenschaftliche Auswahl)

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