Permanent and panerythroid correction of murine beta thalassemia by multiple lentiviral integration in hematopoietic stem cells. - Wikidata - wikimedia - TriplyDB

Permanent and panerythroid correction of murine beta thalassemia by multiple lentiviral integration in hematopoietic stem cells.

Permanent and panerythroid correction of murine beta thalassemia by multiple lentiviral integration in hematopoietic stem cells.

http://www.wikidata.org/entity/Q34393866

about

Transfusion independence and HMGA2 activation after gene therapy of human β-thalassaemia Current and future alternative therapies for beta-thalassemia major Pluripotent stem cells in research and treatment of hemoglobinopathies Hematopoietic stem cell gene therapy:assessing the relevance of preclinical models Hematopoietic stem cell engineering at a crossroads The GATA1-HS2 enhancer allows persistent and position-independent expression of a β-globin transgene Beta-globin LCR and intron elements cooperate and direct spatial reorganization for gene therapy Therapeutic hemoglobin levels after gene transfer in β-thalassemia mice and in hematopoietic cells of β-thalassemia and sickle cells disease patients Gene specificity of suppression of transgene-mediated insertional transcriptional activation by the chicken HS4 insulator.The 3' region of the chicken hypersensitive site-4 insulator has properties similar to its core and is required for full insulator activity.Effects of human gamma-globin in murine beta-thalassaemia.Future alternative therapies for β-thalassemia.Mechanism of reduction in titers from lentivirus vectors carrying large inserts in the 3'LTR.Therapeutic effects of induced pluripotent stem cells in chimeric mice with β-thalassemia.Iron overload cardiomyopathy: better understanding of an increasing disorder.Preclinical evaluation of efficacy and safety of an improved lentiviral vector for the treatment of β-thalassemia and sickle cell disease.Chicken HS4 insulators have minimal barrier function among progeny of human hematopoietic cells transduced with an HIV1-based lentiviral vector.An Erythroid-Specific Chromatin Opening Element Increases β-Globin Gene Expression from Integrated Retroviral Gene Transfer Vectors.High-efficiency transduction of primary human hematopoietic stem cells and erythroid lineage-restricted expression by optimized AAV6 serotype vectors in vitro and in a murine xenograft model in vivo Therapeutic levels of fetal hemoglobin in erythroid progeny of β-thalassemic CD34+ cells after lentiviral vector-mediated gene transfer.Correction of murine β-thalassemia after minimal lentiviral gene transfer and homeostatic in vivo erythroid expansion.Distribution of lentiviral vector integration sites in mice following therapeutic gene transfer to treat β-thalassemia.Allogeneic hematopoietic stem cell transplantation for sickle cell disease: the time is now.The new self-inactivating lentiviral vector for thalassemia gene therapy combining two HPFH activating elements corrects human thalassemic hematopoietic stem cells.Stem cell bioengineering for regenerative medicine.Globin gene transfer as a potential treatment for the beta-thalassaemias and sickle cell disease.A transgenic mouse model expressing exclusively human hemoglobin E: indications of a mild oxidative stress.Functional analysis of erythrocyte determinants of Plasmodium infection High-efficiency transduction of rhesus hematopoietic repopulating cells by a modified HIV1-based lentiviral vector.Chemoselection of allogeneic HSC after murine neonatal transplantation without myeloablation or post-transplant immunosuppression.Ex vivo expansion of normal and chronic myeloid leukemic stem cells without functional alteration using a NUP98HOXA10homeodomain fusion gene.Gene Therapy of the β-Hemoglobinopathies by Lentiviral Transfer of the β(A(T87Q))-Globin Gene.Molecular therapies in beta-thalassaemia.In vivo selection of genetically modified erythroblastic progenitors leads to long-term correction of beta-thalassemia.Gene therapy for hemoglobinopathies: progress and challenges.On the road to gene therapy for beta-thalassemia and sickle cell anemia.Correction of murine sickle cell disease using gamma-globin lentiviral vectors to mediate high-level expression of fetal hemoglobin.Amelioration of murine beta-thalassemia through drug selection of hematopoietic stem cells transduced with a lentiviral vector encoding both gamma-globin and the MGMT drug-resistance gene.A Mouse Model for Human Unstable Hemoglobin Santa Ana.Non-invasive MRI biomarkers for the early assessment of iron overload in a humanized mouse model of β-thalassemia.

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P2860

Permanent and panerythroid correction of murine beta thalassemia by multiple lentiviral integration in hematopoietic stem cells.

http://www.wikidata.org/entity/Q34393866

description

2002 nî lūn-bûn

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2002 թուականի Հոկտեմբերին հրատարակուած գիտական յօդուած

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2002 թվականի հոտեմբերին հրատարակված գիտական հոդված

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2002年の論文

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2002年論文

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2002年論文

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2002年論文

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2002年論文

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2002年論文

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2002年论文

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Permanent and panerythroid cor ...... n in hematopoietic stem cells.

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Permanent and panerythroid cor ...... n in hematopoietic stem cells.

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Permanent and panerythroid cor ...... n in hematopoietic stem cells.

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Permanent and panerythroid cor ...... n in hematopoietic stem cells.

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Permanent and panerythroid cor ...... n in hematopoietic stem cells.

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Permanent and panerythroid cor ...... n in hematopoietic stem cells.

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Permanent and panerythroid cor ...... n in hematopoietic stem cells.

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Permanent and panerythroid cor ...... n in hematopoietic stem cells.

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Proceedings of the National Academy of Sciences of the United States of America

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Permanent and panerythroid cor ...... n in hematopoietic stem cells.

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P2093

Benjamin Cavilla

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Connie J Eaves

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Emmanuel Payen

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Eric E Bouhassira

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Irving M London

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Karen A Westerman

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Louis D Wadsworth

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Mary E Fabry

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R Keith Humphries

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Robert Pawliuk

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P2860

The "beta-like-globin" gene domain in human erythroid cells

Stochastic gene expression in a single cell

The protein CTCF is required for the enhancer blocking activity of vertebrate insulators

Position-independent, high-level expression of the human beta-globin gene in transgenic mice

High expression of human beta S- and alpha-globins in transgenic mice: erythrocyte abnormalities, organ damage, and the effect of hypoxia.

High-level beta-globin expression after retroviral transfer of locus activation region-containing human beta-globin gene derivatives into murine erythroleukemia cells.

The beta-thalassemias.

An erythroid-specific, developmental-stage-independent enhancer far upstream of the human "beta-like globin" genes.

Generation of a high-titer retroviral vector capable of expressing high levels of the human beta-globin gene.

Correction of sickle cell disease in transgenic mouse models by gene therapy.

P304

14380-14385

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scholarly article

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10.1073/PNAS.212507099

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P433

22

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P478

99

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Philippe Leboulch

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2002-10-21T00:00:00Z

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11071631

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12391330

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137892

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