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  1. Article ; Online: Erythroleukemia: all roads lead to GATA1?

    Strouboulis, John

    Blood

    2020  Volume 136, Issue 6, Page(s) 648–649

    MeSH term(s) GATA1 Transcription Factor/genetics ; GATA1 Transcription Factor/metabolism ; Humans ; Leukemia, Erythroblastic, Acute/genetics ; Transcription Factors/genetics ; Transcriptome
    Chemical Substances GATA1 Transcription Factor ; GATA1 protein, human ; Transcription Factors
    Language English
    Publishing date 2020-08-05
    Publishing country United States
    Document type Journal Article ; Comment
    ZDB-ID 80069-7
    ISSN 1528-0020 ; 0006-4971
    ISSN (online) 1528-0020
    ISSN 0006-4971
    DOI 10.1182/blood.2020006107
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  2. Article ; Online: The effects of chronic glucorticoid stimulation on erythropoiesis in Cushing syndrome.

    Strouboulis, John / El Hoss, Sara

    Haematologica

    2023  Volume 108, Issue 4, Page(s) 947–948

    MeSH term(s) Humans ; Cushing Syndrome/diagnosis ; Erythropoiesis
    Language English
    Publishing date 2023-04-01
    Publishing country Italy
    Document type Editorial ; Comment
    ZDB-ID 2333-4
    ISSN 1592-8721 ; 0017-6567 ; 0390-6078
    ISSN (online) 1592-8721
    ISSN 0017-6567 ; 0390-6078
    DOI 10.3324/haematol.2022.281355
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article ; Online: GATA1: function through disorder.

    Strouboulis, John / Ronchi, Antonella E

    Blood

    2022  Volume 139, Issue 16, Page(s) 2422–2423

    MeSH term(s) Humans ; GATA1 Transcription Factor/genetics ; Down Syndrome ; Leukemia, Megakaryoblastic, Acute ; Anemia
    Chemical Substances GATA1 Transcription Factor ; GATA1 protein, human
    Language English
    Publishing date 2022-04-04
    Publishing country United States
    Document type Editorial ; Comment
    ZDB-ID 80069-7
    ISSN 1528-0020 ; 0006-4971
    ISSN (online) 1528-0020
    ISSN 0006-4971
    DOI 10.1182/blood.2021015351
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  4. Article ; Online: Recent Approaches for Manipulating Globin Gene Expression in Treating Hemoglobinopathies.

    Mussolino, Claudio / Strouboulis, John

    Frontiers in genome editing

    2021  Volume 3, Page(s) 618111

    Abstract: Tissue oxygenation throughout life depends on the activity of hemoglobin (Hb) one of the hemeproteins that binds oxygen in the lungs and secures its delivery throughout the body. Hb is composed of four monomers encoded by eight different genes the ... ...

    Abstract Tissue oxygenation throughout life depends on the activity of hemoglobin (Hb) one of the hemeproteins that binds oxygen in the lungs and secures its delivery throughout the body. Hb is composed of four monomers encoded by eight different genes the expression of which is tightly regulated during development, resulting in the formation of distinct hemoglobin tetramers in each developmental stage. Mutations that alter hemoglobin structure or its regulated expression result in a large group of diseases typically referred to as hemoglobinopathies that are amongst the most common genetic defects worldwide. Unprecedented efforts in the last decades have partially unraveled the complex mechanisms that control globin gene expression throughout development. In addition, genome wide association studies have revealed protective genetic traits capable of ameliorating the clinical manifestations of severe hemoglobinopathies. This knowledge has fueled the exploration of innovative therapeutic approaches aimed at modifying the genome or the epigenome of the affected cells to either restore hemoglobin function or to mimic the effect of protective traits. Here we describe the key steps that control the switch in gene expression that concerns the different globin genes during development and highlight the latest efforts in altering globin regulation for therapeutic purposes.
    Language English
    Publishing date 2021-08-02
    Publishing country Switzerland
    Document type Journal Article ; Review
    ISSN 2673-3439
    ISSN (online) 2673-3439
    DOI 10.3389/fgeed.2021.618111
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  5. Article ; Online: A novel index to evaluate ineffective erythropoiesis in hematological diseases offers insights into sickle cell disease.

    Brewin, John / El Hoss, Sara / Strouboulis, John / Rees, David

    Haematologica

    2022  Volume 107, Issue 1, Page(s) 338–341

    MeSH term(s) Anemia, Sickle Cell/complications ; Erythrocytes ; Erythropoiesis ; Humans
    Language English
    Publishing date 2022-01-01
    Publishing country Italy
    Document type Journal Article
    ZDB-ID 2333-4
    ISSN 1592-8721 ; 0017-6567 ; 0390-6078
    ISSN (online) 1592-8721
    ISSN 0017-6567 ; 0390-6078
    DOI 10.3324/haematol.2021.279623
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  6. Article ; Online: Preface to IUBMB life special issue on GATA transcription factors in development, differentiation, and disease.

    Strouboulis, John / Crispino, John D

    IUBMB life

    2019  Volume 72, Issue 1, Page(s) 8–9

    MeSH term(s) Animals ; Cell Differentiation ; GATA Transcription Factors/genetics ; GATA Transcription Factors/metabolism ; Humans ; Leukemia/genetics ; Leukemia/metabolism ; Leukemia/pathology ; Molecular Biology ; Periodicals as Topic
    Chemical Substances GATA Transcription Factors
    Language English
    Publishing date 2019-11-28
    Publishing country England
    Document type Introductory Journal Article
    ZDB-ID 1492141-8
    ISSN 1521-6551 ; 1521-6543
    ISSN (online) 1521-6551
    ISSN 1521-6543
    DOI 10.1002/iub.2205
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    Zs.A 1611: Show issues Location:
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  7. Article ; Online: Revolutionising healing: Gene Editing's breakthrough against sickle cell disease.

    Dimitrievska, Marija / Bansal, Dravie / Vitale, Marta / Strouboulis, John / Miccio, Annarita / Nicolaides, Kypros H / El Hoss, Sara / Shangaris, Panicos / Jacków-Malinowska, Joanna

    Blood reviews

    2024  Volume 65, Page(s) 101185

    Abstract: Recent advancements in gene editing illuminate new potential therapeutic approaches for Sickle Cell Disease (SCD), a debilitating monogenic disorder caused by a point mutation in the β-globin gene. Despite the availability of several FDA-approved ... ...

    Abstract Recent advancements in gene editing illuminate new potential therapeutic approaches for Sickle Cell Disease (SCD), a debilitating monogenic disorder caused by a point mutation in the β-globin gene. Despite the availability of several FDA-approved medications for symptomatic relief, allogeneic hematopoietic stem cell transplantation (HSCT) remains the sole curative option, underscoring a persistent need for novel treatments. This review delves into the growing field of gene editing, particularly the extensive research focused on curing haemoglobinopathies like SCD. We examine the use of techniques such as CRISPR-Cas9 and homology-directed repair, base editing, and prime editing to either correct the pathogenic variant into a non-pathogenic or wild-type one or augment fetal haemoglobin (HbF) production. The article elucidates ways to optimize these tools for efficacious gene editing with minimal off-target effects and offers insights into their effective delivery into cells. Furthermore, we explore clinical trials involving alternative SCD treatment strategies, such as LentiGlobin therapy and autologous HSCT, distilling the current findings. This review consolidates vital information for the clinical translation of gene editing for SCD, providing strategic insights for investigators eager to further the development of gene editing for SCD.
    MeSH term(s) Humans ; Gene Editing/methods ; CRISPR-Cas Systems ; Anemia, Sickle Cell/genetics ; Anemia, Sickle Cell/therapy ; Hemoglobinopathies/genetics ; Fetal Hemoglobin/genetics
    Chemical Substances Fetal Hemoglobin (9034-63-3)
    Language English
    Publishing date 2024-03-07
    Publishing country England
    Document type Journal Article ; Review
    ZDB-ID 639015-8
    ISSN 1532-1681 ; 0268-960X
    ISSN (online) 1532-1681
    ISSN 0268-960X
    DOI 10.1016/j.blre.2024.101185
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  8. Article ; Online: Translational regulation and deregulation in erythropoiesis.

    Vatikioti, Alexandra / Karkoulia, Elena / Ioannou, Marina / Strouboulis, John

    Experimental hematology

    2019  Volume 75, Page(s) 11–20

    Abstract: Translational regulation plays a critical role in erythropoiesis, as it reflects the translational needs of enucleated mature erythroid cells in the absence of transcription and the large translational demands of balanced globin chain synthesis during ... ...

    Abstract Translational regulation plays a critical role in erythropoiesis, as it reflects the translational needs of enucleated mature erythroid cells in the absence of transcription and the large translational demands of balanced globin chain synthesis during erythroid maturation. In addition, red blood cells need to respond quickly to changes in their environment and the demands of the organism. Translational regulation occurs at several levels in erythroid cells, including the differential utilization of upstream open reading frames during differentiation and in response to signaling and the employment of RNA-binding proteins in an erythroid cell-specific fashion. Translation initiation is a critical juncture for translational regulation in response to environmental signals such as heme and iron availability, whereas regulatory mechanisms for ribosome recycling are consistent with recent observations highlighting the importance of maintaining adequate ribosome levels in differentiating erythroid cells. Translational deregulation in erythroid cells leads to disease associated with ineffective erythropoiesis, further highlighting the pivotal role translational regulation in erythropoiesis plays in human physiology and homeostasis. Overall, erythropoiesis has served as a unique model that has provided invaluable insight into translational regulation.
    MeSH term(s) Cell Differentiation/physiology ; Erythroid Cells/cytology ; Erythroid Cells/metabolism ; Erythropoiesis/physiology ; Heme/metabolism ; Humans ; Iron/metabolism ; Protein Biosynthesis/physiology ; RNA-Binding Proteins/metabolism ; Ribosomes/metabolism ; Signal Transduction/physiology
    Chemical Substances RNA-Binding Proteins ; Heme (42VZT0U6YR) ; Iron (E1UOL152H7)
    Language English
    Publishing date 2019-05-30
    Publishing country Netherlands
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 185107-x
    ISSN 1873-2399 ; 0531-5573 ; 0301-472X
    ISSN (online) 1873-2399
    ISSN 0531-5573 ; 0301-472X
    DOI 10.1016/j.exphem.2019.05.004
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    Zs.A 922: Show issues Location:
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  9. Article: The Pleiotropic Effects of GATA1 and KLF1 in Physiological Erythropoiesis and in Dyserythropoietic Disorders.

    Barbarani, Gloria / Fugazza, Cristina / Strouboulis, John / Ronchi, Antonella E

    Frontiers in physiology

    2019  Volume 10, Page(s) 91

    Abstract: In the last few years, the advent of new technological approaches has led to a better knowledge of the ontogeny of erythropoiesis during development and of the journey leading from hematopoietic stem cells (HSCs) to mature red blood cells (RBCs). Our ... ...

    Abstract In the last few years, the advent of new technological approaches has led to a better knowledge of the ontogeny of erythropoiesis during development and of the journey leading from hematopoietic stem cells (HSCs) to mature red blood cells (RBCs). Our view of a well-defined hierarchical model of hematopoiesis with a near-homogeneous HSC population residing at the apex has been progressively challenged in favor of a landscape where HSCs themselves are highly heterogeneous and lineages separate earlier than previously thought. The coordination of these events is orchestrated by transcription factors (TFs) that work in a combinatorial manner to activate and/or repress their target genes. The development of next generation sequencing (NGS) has facilitated the identification of pathological mutations involving TFs underlying hematological defects. The examples of GATA1 and KLF1 presented in this review suggest that in the next few years the number of TF mutations associated with dyserythropoietic disorders will further increase.
    Language English
    Publishing date 2019-02-12
    Publishing country Switzerland
    Document type Journal Article ; Review
    ZDB-ID 2564217-0
    ISSN 1664-042X
    ISSN 1664-042X
    DOI 10.3389/fphys.2019.00091
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  10. Article ; Online: Males with sickle cell disease have higher risks of cerebrovascular disease, increased inflammation, and a reduced response to hydroxyurea.

    Di Mauro, Margherita / El Hoss, Sara / Nardo-Marino, Amina / Stuart-Smith, Sara / Strouboulis, John / Gibson, John S / Rees, David C / Brewin, John N

    American journal of hematology

    2023  Volume 98, Issue 11, Page(s) E341–E344

    Abstract: Biological sex is important. Male sex is associated with worse outcomes in most measures, including cerebrovascular disease, hospital admissions, and blood transfusions, but not survival. Females also appear to have a better response to hydroxyurea ... ...

    Abstract Biological sex is important. Male sex is associated with worse outcomes in most measures, including cerebrovascular disease, hospital admissions, and blood transfusions, but not survival. Females also appear to have a better response to hydroxyurea therapy, reduced markers of inflammation, and better liver function.
    MeSH term(s) Female ; Male ; Humans ; Hydroxyurea ; Antisickling Agents ; Anemia, Sickle Cell/complications ; Cerebrovascular Disorders ; Blood Transfusion
    Chemical Substances Hydroxyurea (X6Q56QN5QC) ; Antisickling Agents
    Language English
    Publishing date 2023-08-30
    Publishing country United States
    Document type Letter
    ZDB-ID 196767-8
    ISSN 1096-8652 ; 0361-8609
    ISSN (online) 1096-8652
    ISSN 0361-8609
    DOI 10.1002/ajh.27074
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