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Articles de revues sur le sujet « Globin switching »

Auteur : Grafiati

Publié le 9 mars 2023

Mis à jour le 31 juillet 2025

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1

Ikuta, Tohru, Thalia Papayannopoulou, George Stamatoyannopoulos, and Yuet Wai Kan. "Globin Gene Switching." Journal of Biological Chemistry 271, no. 24 (1996): 14082–91. http://dx.doi.org/10.1074/jbc.271.24.14082.

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Wood, WG. "Haemoglobin Switching." Physiology 3, no. 1 (1988): 33–35. http://dx.doi.org/10.1152/physiologyonline.1988.3.1.33.

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Haemoglobin switching involves changes in production of the globin chains at specific times during vertebrate development. The hereditary haemolytic anaemias known as thalassaemias, which result from decreased or no synthesis of one of the globins, are some of the most common genetic diseases of humans.

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3

Kingsley, Paul D., Jeffrey Malik, Rachel L. Emerson, et al. "“Maturational” globin switching in primary primitive erythroid cells." Blood 107, no. 4 (2006): 1665–72. http://dx.doi.org/10.1182/blood-2005-08-3097.

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Mammals have 2 distinct erythroid lineages. The primitive erythroid lineage originates in the yolk sac and generates a cohort of large erythroblasts that terminally differentiate in the bloodstream. The definitive erythroid lineage generates smaller enucleated erythrocytes that become the predominant cell in fetal and postnatal circulation. These lineages also have distinct globin expression patterns. Our studies in primary murine primitive erythroid cells indicate that βH1 is the predominant β-globin transcript in the early yolk sac. Thus, unlike the human, murine β-globin genes are not up-re

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4

Perrine, Susan P. "Switching globin, raising red cells." Blood 118, no. 4 (2011): 834–36. http://dx.doi.org/10.1182/blood-2011-06-354373.

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Johnson, Robert M., Deborah Gumucio, and Morris Goodman. "Globin gene switching in primates." Comparative Biochemistry and Physiology Part A: Molecular & Integrative Physiology 133, no. 3 (2002): 877–83. http://dx.doi.org/10.1016/s1095-6433(02)00205-2.

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6

Hsia, Nelson, Jennifer L. Axe, Noelle Paffett-Lugassy, Yi Zhou, and Leonard I. Zon. "Globin switching in the zebrafish." Blood Cells, Molecules, and Diseases 38, no. 2 (2007): 145. http://dx.doi.org/10.1016/j.bcmd.2006.10.062.

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Roberts, N. A., J. A. Sloane-Stanley, J. A. Sharpe, S. J. Stanworth, and W. G. Wood. "Globin Gene Switching in Transgenic Mice Carrying HS2-Globin Gene Constructs." Blood 89, no. 2 (1997): 713–23. http://dx.doi.org/10.1182/blood.v89.2.713.

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Abstract We have examined the pattern of human globin gene switching in transgenic mice containing three different γ and β gene constructs (HS2GγAγδβ, HS2Aγβneo, and HS2Aγenβ) and compared the results with previously described transgenics (HS2Aγβ, HS2GγAγ-117δβ, and LCRεGγAγδβ). Developmental regulation was observed in all cases with identical patterns in lines bearing the same construct. Three different patterns of switching were observed: LCRεGγAγδβ and HS2Aγβneo mice switched rapidly, HS2GγAγδβ and HS2GγAγ-117δβ at an intermediate rate, and HS2Aγβ and HS2Aγenβ mice showed delayed switching,

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Palis, James, Jeff Malik, Rachael L. Emerson, et al. "“Maturational” Globin Switching in Primary Primitive Erythroid Cells." Blood 106, no. 11 (2005): 3634. http://dx.doi.org/10.1182/blood.v106.11.3634.3634.

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Abstract Mammals have two distinct erythroid lineages. The “definitive” erythroid lineage generates small, enucleated erythrocytes that constitute the predominant cell type in the fetal and postnatal circulation. It is preceded by the “primitive” erythroid lineage, which originates in the yolk sac and generates a semi-synchronous wave of large erythroblasts that terminally differentiate in the bloodstream. This feature provides a unique opportunity to investigate changes in gene expression during erythroid maturation. Here, we have examined expression of the various α- and β-globin genes in pu

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Chan, Fung-Yee, Judith Robinson, Alison Brownlie та ін. "Characterization of Adult α- and β-Globin Genes in the Zebrafish". Blood 89, № 2 (1997): 688–700. http://dx.doi.org/10.1182/blood.v89.2.688.

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Abstract Developmental switching of hemoglobins (Hbs) occurs in most vertebrates, yet the cellular and molecular basis for this process remains elusive. The zebrafish is a new genetic and developmental system that can be used to study embryogenesis, and mutants with a variety of defects in hematopoiesis have recently been derived. To initiate our studies on Hb switching in this organism, we have characterized the globins expressed in the adult. Reversed-phase high performance liquid chromatography and mass spectrometric analyses of adult peripheral blood hemolysates showed that there are three

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Xu, Jian, Vijay G. Sankaran, Yuko Fujiwara, and Stuart H. Orkin. "Control of Hemoglobin Switching by BCL11A." Blood 114, no. 22 (2009): 5. http://dx.doi.org/10.1182/blood.v114.22.5.5.

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Abstract Abstract 5 All vertebrates switch expression of globin chains during development. In humans b-like globins switch from embryonic to fetal to adult, whereas in the mouse a single switch from embryonic to adult occurs. The switch from human fetal (g) to adult (b) expression is especially critical in the b-hemoglobin disorders, such as sickle cell anemia and the b-thalassemias. Delay of the switch or reactivation of the fetal gene in the adult stage greatly ameliorates clinical severity. Despite intensive molecular studies of the human b-globin cluster over more than two decades, the pro

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11

Tuan, Dorothy. "ERV-9 LTR Retrotransposon Modulates Globin Gene Switching." Blood 132, Supplement 1 (2018): 2341. http://dx.doi.org/10.1182/blood-2018-99-117280.

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Abstract In the human beta-globin gene locus, an LTR retrotransposon derived from ERV-9 human endogenous retrovirus is located near the locus control region (LCR) far upstream of the globin genes. In transgenic mice carrying the 100 kb human globin gene locus, deleting the ERV-9 LTR by cre-loxP mediated in situ recombination inactivates transcription of beta-globin gene by ~50% and activates that of gamma-globin gene by up to 5 fold, to at least 20% the level of beta-globin mRNA in both fetal and adult erythroid cells. Chromosome-conformation-capture (3C) shows that the ERV-9 LTR preferentiall

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12

Grosveld, F., M. Antoniou, M. Berry, et al. "Regulation of Human Globin Gene Switching." Cold Spring Harbor Symposia on Quantitative Biology 58 (January 1, 1993): 7–13. http://dx.doi.org/10.1101/sqb.1993.058.01.004.

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13

Hebbes, Tim R., Alan W. Thorne, Alison L. Clayton, and Colyn Crane-Robinson. "Histone acetylation and globin gene switching." Nucleic Acids Research 20, no. 5 (1992): 1017–22. http://dx.doi.org/10.1093/nar/20.5.1017.

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Beauchemin, Hugues, and Marie Trudel. "Evidence for a Bigenic Chromatin Subdomain in Regulation of the Fetal-to-Adult Hemoglobin Switch." Molecular and Cellular Biology 29, no. 6 (2008): 1635–48. http://dx.doi.org/10.1128/mcb.01735-08.

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ABSTRACT During development, human β-globin locus regulation undergoes two critical switches, the embryonic-to-fetal and fetal-to-adult hemoglobin switches. To define the role of the fetal Aγ-globin promoter in switching, human β-globin-YAC transgenic mice were produced with the Aγ-globin promoter replaced by the erythroid porphobilinogen deaminase (PBGD) promoter (PBGDAγ-YAC). Activation of the stage-independent PBGDAγ-globin strikingly stimulated native Gγ-globin expression at the fetal and adult stages, identifying a fetal gene pair or bigenic cooperative mechanism. This impaired fetal sile

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15

Habara, Alawi. "Exploratory Review and In Silico Insights into circRNA and RNA-Binding Protein Roles in γ-Globin to β-Globin Switching". Cells 14, № 4 (2025): 312. https://doi.org/10.3390/cells14040312.

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β-globin gene cluster regulation involves complex mechanisms to ensure proper expression and function in RBCs. During development, switching occurs as γ-globin is replaced by β-globin. Key regulators, like BCL11A and ZBTB7A, repress γ-globin expression to facilitate this transition with other factors, like KLF1, LSD1, and PGC-1α; these regulators ensure an orchestrated transition from γ- to β-globin during development. While these mechanisms have been extensively studied, circRNAs have recently emerged as key contributors to gene regulation, but their role in β-globin gene cluster regulation r

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Bank, Arthur. "Regulation of human fetal hemoglobin: new players, new complexities." Blood 107, no. 2 (2006): 435–43. http://dx.doi.org/10.1182/blood-2005-05-2113.

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AbstractThe human globin genes are among the most extensively characterized in the human genome, yet the details of the molecular events regulating normal human hemoglobin switching and the potential reactivation of fetal hemoglobin in adult hematopoietic cells remain elusive. Recent discoveries demonstrate physical interactions between the β locus control region and the downstream structural γ- and β-globin genes, and with transcription factors and chromatin remodeling complexes. These interactions all play roles in globin gene expression and globin switching at the human β-globin locus. If t

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17

McConnell, Sean C., Yongliang Huo, Shan-Run Liu, Ting-Ting Zhang, Clayton L. Ulrey, and Thomas M. Ryan. "Human Gamma Globin Gene Regulation in Knock-In Mouse Models of Anemia." Blood 110, no. 11 (2007): 1779. http://dx.doi.org/10.1182/blood.v110.11.1779.1779.

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Abstract The generation of transgenic and gene targeted mouse models of human hemoglobinopathies provides valuable opportunities to test mechanisms of human globin gene regulation and experimental therapies. Yet mice do not naturally have a fetal hemoglobin, challenging our ability to adequately model the developmental onset of disease. Transgenic model systems that contain the entire human β-globin locus present obstacles to the study of human globin gene switching, including a fetal to adult globin gene switch that occurs too early in development. The generation of genetically engineered mic

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Sabatino, Denise E., Amanda P. Cline, Patrick G. Gallagher та ін. "Substitution of the Human β-Spectrin Promoter for the Human Aγ-Globin Promoter Prevents Silencing of a Linked Human β-Globin Gene in Transgenic Mice". Molecular and Cellular Biology 18, № 11 (1998): 6634–40. http://dx.doi.org/10.1128/mcb.18.11.6634.

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ABSTRACT During development, changes occur in both the sites of erythropoiesis and the globin genes expressed at each developmental stage. Previous work has shown that high-level expression of human β-like globin genes in transgenic mice requires the presence of the locus control region (LCR). Models of hemoglobin switching propose that the LCR and/or stage-specific elements interact with globin gene sequences to activate specific genes in erythroid cells. To test these models, we generated transgenic mice which contain the human Aγ-globin gene linked to a 576-bp fragment containing the human

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19

Papadopoulos, Petros, Athanassia Kafasi, Cuyper Iris M. De та ін. "Mild dyserythropoiesis and β-like globin gene expression imbalance due to the loss of histone chaperone ASF1B". Human Genomics 14, № 1 (2020): 39. https://doi.org/10.1186/s40246-020-00283-3.

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The expression of the human β-like globin genes follows a well-orchestrated developmental pattern, undergoing two essential switches, the first one during the first weeks of gestation (ε to γ), and the second one during the perinatal period (γ to β). The γ- to β-globin gene switching mechanism includes suppression of fetal (γ-globin, HbF) and activation of adult (β-globin, HbA) globin gene transcription. In hereditary persistence of fetal hemoglobin (HPFH), the γ-globin suppression mechanism is impaired leaving these individuals with unusual elevated levels of fetal hemoglobin (HbF) in adultho

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Lowrey, Christopher. "Another piece of the globin-switching puzzle." Blood 107, no. 5 (2006): 1744. http://dx.doi.org/10.1182/blood-2005-12-4896.

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21

ENVER, T., and D. GREAVES. "Globin gene switching: A paradigm or what?" Current Opinion in Biotechnology 2, no. 6 (1991): 787–95. http://dx.doi.org/10.1016/s0958-1669(05)80108-9.

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Enver, Tariq, and David R. Greaves. "Globin gene switching — a paradigm or what?" Current Biology 2, no. 3 (1992): 145. http://dx.doi.org/10.1016/0960-9822(92)90262-9.

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23

Choi, Ok-Ryun Baik, та James Douglas Engel. "Developmental regulation of β-globin gene switching". Cell 55, № 1 (1988): 17–26. http://dx.doi.org/10.1016/0092-8674(88)90005-0.

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Orkin, Stuart H. "Globin gene regulation and switching: Circa 1990." Cell 63, no. 4 (1990): 665–72. http://dx.doi.org/10.1016/0092-8674(90)90133-y.

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25

Zitnik, G., Q. Li, G. Stamatoyannopoulos, and T. Papayannopoulou. "Serum factors can modulate the developmental clock of gamma- to beta-globin gene switching in somatic cell hybrids." Molecular and Cellular Biology 13, no. 8 (1993): 4844–51. http://dx.doi.org/10.1128/mcb.13.8.4844-4851.1993.

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The fusion of human fetal erythroid (HFE) cells with mouse erythroleukemia (MEL) cells produces stable synkaryons (HFE x MEL) which can be monitored for extended periods of time in culture. Initially these hybrids express a human fetal globin program (gamma >> beta), but after weeks or months in culture, they switch to an adult pattern of globin expression (beta >> gamma). The rate at which hybrids switch to the adult phenotype is roughly dependent on the gestational age of the fetal erythroid cells used in the fusion, suggesting that the rate of switching in vitro may be determine

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Zitnik, G., Q. Li, G. Stamatoyannopoulos, and T. Papayannopoulou. "Serum factors can modulate the developmental clock of gamma- to beta-globin gene switching in somatic cell hybrids." Molecular and Cellular Biology 13, no. 8 (1993): 4844–51. http://dx.doi.org/10.1128/mcb.13.8.4844.

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The fusion of human fetal erythroid (HFE) cells with mouse erythroleukemia (MEL) cells produces stable synkaryons (HFE x MEL) which can be monitored for extended periods of time in culture. Initially these hybrids express a human fetal globin program (gamma >> beta), but after weeks or months in culture, they switch to an adult pattern of globin expression (beta >> gamma). The rate at which hybrids switch to the adult phenotype is roughly dependent on the gestational age of the fetal erythroid cells used in the fusion, suggesting that the rate of switching in vitro may be determine

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Marongiu, Maria F., Susanna Porcu, Daniela Poddie та ін. "Different Hemoglobin Switching Pattern of β-Thalassemia Mutations at the Proximal and Distal Human β-Globin CACCC Box." Blood 110, № 11 (2007): 1780. http://dx.doi.org/10.1182/blood.v110.11.1780.1780.

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Abstract The CACCC box is duplicated in the β globin gene promoter of humans and other mammals. While the function of the proximal element as a binding site for EKLF has already been well established, the role of the distal element remains unclear The distal CACCC box has been previously reported not to bind EKLF in vitro. A minor role of the distal CACCC element in β globin gene promoter function is suggested by the observation that naturally occurring β thalassemia mutations affecting the proximal CACCC box are far more severe than those affecting the distal element. Nevertheless recent evid

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Esteghamat, Fatemehsadat, Nynke Gillemans, Ivan Bilic, et al. "Erythropoiesis and Globin Switching in Compound Klf1::Bcl11a mutant mice." Blood 120, no. 21 (2012): 1019. http://dx.doi.org/10.1182/blood.v120.21.1019.1019.

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Abstract Abstract 1019 Reactivation of fetal γ-globin is of outstanding demand in patients with β-hemoglobinopathies. B-Cell/Lymphoma 11A (BCL11A) is a well-known repressor of γ-globin, and its expression is directly activated by Kruppel-Like Factor 1 (KLF1). KLF1 is a major regulator of human fetal to adult hemoglobin switching and reduced expression of KLF1 due to mutations is associated with hereditary persistence of fetal hemoglobin (HPFH). Analysis of the HPFH phenotype has led to the proposal that KLF1 has a dual role in γ-globin suppression, through its preferential activation of the β-

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Ganis, Jared J., Elizabeth B. Riley, James Palis, and Leonard I. Zon. "A Screen for Regulators of Globin Switching in the Zebrafish Embryo." Blood 120, no. 21 (2012): 826. http://dx.doi.org/10.1182/blood.v120.21.826.826.

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Abstract Abstract 826 The switching of the globin genes involves critical transcriptional regulators such as BCL11A, EKLF and SOX6, and the induction of fetal globin has been shown to ameliorate the symptoms of diseases such as sickle cell anemia. Recently, there has been interest in driving iPS cells to produce mature red cells that express adult globin genes in an attempt to make these cells therapeutically useful. Here, to understand hemoglobin switching and the molecular pathways that allow the establishment of an adult fate in embryonic tissues, we utilized a screening approach in the zeb

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Harju, Susanna, Kellie J. McQueen та Kenneth R. Peterson. "Chromatin Structure and Control of β-Like Globin Gene Switching". Experimental Biology and Medicine 227, № 9 (2002): 683–700. http://dx.doi.org/10.1177/153537020222700902.

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The human β-globin locus is a complex genetic system widely used for analysis of eukaryotic gene expression. The locus consists of five functional β-like globin genes, ε, Gγ, Aγ, δ, and β, arrayed on the chromosome in the order that they are expressed during ontogeny. Globin gene expression is regulated, in part, by the locus control region, which physically consists of five DNasel-hypersensitive sites located 6-22 Kb upstream of the ε-globin gene. During ontogeny two switches occur in β-globin gene expression that reflect the changing oxygen requirements of the fetus. The first switch from em

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Guo, Xiang, Jennifer Plank-Bazinet, Ivan Krivega, Ryan K. Dale, and Ann Dean. "Embryonic erythropoiesis and hemoglobin switching require transcriptional repressor ETO2 to modulate chromatin organization." Nucleic Acids Research 48, no. 18 (2020): 10226–40. http://dx.doi.org/10.1093/nar/gkaa736.

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Abstract The underlying mechanism of transcriptional co-repressor ETO2 during early erythropoiesis and hemoglobin switching is unclear. We find that absence of ETO2 in mice interferes with down-regulation of PU.1 and GATA2 in the fetal liver, impeding a key step required for commitment to erythroid maturation. In human β-globin transgenic Eto2 null mice and in human CD34+ erythroid progenitor cells with reduced ETO2, loss of ETO2 results in ineffective silencing of embryonic/fetal globin gene expression, impeding hemoglobin switching during erythroid differentiation. ETO2 occupancy genome-wide

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Wang, Wentian, Yuanyuan Tuo, Yuchen Gao та ін. "TGF-β1 Reverses Hemoglobin Switching in Erythroid Progenitor Cells before Erythropoietin Induction". Blood 144, Supplement 1 (2024): 2474. https://doi.org/10.1182/blood-2024-204590.

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Objective: This study aims to elucidate the pattern and mechanism by which Transforming Growth Factor-β1 (TGF-β1) regulates human hemoglobin switching, providing foundational evidence for subsequent clinical translational research. Methods: Human umbilical cord blood CD34+ hematopoietic stem and progenitor cells (HSPCs) were enriched using magnetic beads and subjected to a biphasic erythroid in vitro culture. The effect of TGF-β1 on globin switching was assessed at various stages of erythroid differentiation: the EPO-independent erythroid progenitor cell stage, the EPO-dependent erythroid prec

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Felice, Alexander E. "KLF1 Dependent Pathways In Developmental Globin Gene Switching." Blood 116, no. 21 (2010): 5162. http://dx.doi.org/10.1182/blood.v116.21.5162.5162.

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Abstract Abstract 5162 We provide additional data on members of the family from Malta with Hereditary Persistence of Fetal Hemoglobin (HPFH) due to KLF1 haplo-insufficiency. The data indicated a possible role of additional loci in the pathway of globin gene control. We showed that KLF1 functions as a master regulator of erythropoiesis and developmental globin gene switching (Borg et al., Nature Genetics doi: 10. 1038/ng.630, 2010), at least partly through BCL11A. Given the phenoytpes of the HPFH heterozygotes, the truncating KLF1 p.K288X was best described as a dominant mutation with variable

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Mookerjee, B., MO Arcasoy, and GF Atweh. "Spontaneous delta- to beta-globin switching in K562 human leukemia cells." Blood 79, no. 3 (1992): 820–25. http://dx.doi.org/10.1182/blood.v79.3.820.820.

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Abstract Previous analysis of the hemoglobin phenotype of the K562 human erythroleukemia cell line showed regulated expression of the epsilon-, zeta-, gamma-, alpha-, and delta-globin genes. Expression of the beta- globin genes has not been previously detected in this cell line. In this report, we describe the isolation of a variant of the K562 cell line that actively expresses beta-globin messenger RNA (mRNA) and polypeptide and shows greatly reduced expression of the delta-globin genes. This phenotype developed spontaneously in culture while two other K562 isolates grown under the same cultu

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Mookerjee, B., MO Arcasoy, and GF Atweh. "Spontaneous delta- to beta-globin switching in K562 human leukemia cells." Blood 79, no. 3 (1992): 820–25. http://dx.doi.org/10.1182/blood.v79.3.820.bloodjournal793820.

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Previous analysis of the hemoglobin phenotype of the K562 human erythroleukemia cell line showed regulated expression of the epsilon-, zeta-, gamma-, alpha-, and delta-globin genes. Expression of the beta- globin genes has not been previously detected in this cell line. In this report, we describe the isolation of a variant of the K562 cell line that actively expresses beta-globin messenger RNA (mRNA) and polypeptide and shows greatly reduced expression of the delta-globin genes. This phenotype developed spontaneously in culture while two other K562 isolates grown under the same culture condit

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Tumburu, Laxminath, Colleen Byrnes, Y. Terry Lee, Jaira F. de Vasconcellos, Antoinette Rabel, and Jeffery L. Miller. "IGF2BP1 Reverses Hemoglobin Switching in Adult Erythroblasts." Blood 126, no. 23 (2015): 639. http://dx.doi.org/10.1182/blood.v126.23.639.639.

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Abstract During human ontogeny, high-level transcription within the beta-globin gene cluster switches sequentially from embryonic-to-fetal-to-adult genes. Beta-thalassemias and sickle-cell disease are manifested by reduced or mutated expression of the adult-stage, beta-globin gene. Research is aimed toward the eventual therapeutic goal of safely preventing or reversing the fetal-to-adult hemoglobin switch among these patient populations. To identify genes that may be involved in regulation of the fetal-to-adult erythroid switch, purified CD34(+) cells from six umbilical cord (fetal) and six ad

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Caria, Cristian Antonio, Valeria Faà, and Maria Serafina Ristaldi. "Krüppel-Like Factor 1: A Pivotal Gene Regulator in Erythropoiesis." Cells 11, no. 19 (2022): 3069. http://dx.doi.org/10.3390/cells11193069.

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Krüppel-like factor 1 (KLF1) plays a crucial role in erythropoiesis. In-depth studies conducted on mice and humans have highlighted its importance in erythroid lineage commitment, terminal erythropoiesis progression and the switching of globin genes from γ to β. The role of KLF1 in haemoglobin switching is exerted by the direct activation of β-globin gene and by the silencing of γ-globin through activation of BCL11A, an important γ-globin gene repressor. The link between KLF1 and γ-globin silencing identifies this transcription factor as a possible therapeutic target for β-hemoglobinopathies.

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Moi, Paolo, Loredana Porcu, Maria G. Marini та ін. "Differential Modulation of the β-Like Globin Genes by KLFs Isolated with a γ-Globin CACCC Bait." Blood 106, № 11 (2005): 3637. http://dx.doi.org/10.1182/blood.v106.11.3637.3637.

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Abstract The globin CACCC boxes are absolutely required for the appropriate regulation of the β-like globin genes. While the β-globin CACCC box binds EKLF/KLF1, a likely adult switching factor, analogous factors, interacting with the γ-globin gene and predicted to regulate the fetal stage of hemoglobin switching, have so far been elusive. By using yeast one hybrid assay, we have isolated four KLFs, KLF1, 2, 4, and 6, that bound the γ-CACCC bait. To establish their role in globin regulation and in the switching of hemoglobins, these factors were compared to four other KLFs already established o

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Esteghamat, Fatemehsadat, Nynke Gillemans, Ivan Bilic, et al. "Erythropoiesis and globin switching in compound Klf1::Bcl11a mutant mice." Blood 121, no. 13 (2013): 2553–62. http://dx.doi.org/10.1182/blood-2012-06-434530.

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Key Points Our data support an important role for the KLF1-BCL11A axis in erythroid maturation and hemoglobin switching. In adults, gamma-globin levels decline in Bcl11a and Klf1::Bcl11a mutants, suggesting an additional layer of gamma-globin silencing.

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Grosveld, F. "Control of globin gene switching and the search for foetal globin activating compounds." Journal of Pharmacy and Pharmacology 50, S9 (1998): 25. http://dx.doi.org/10.1111/j.2042-7158.1998.tb02225.x.

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41

Lloyd, J. A., J. M. Krakowsky, S. C. Crable, and J. B. Lingrel. "Human gamma- to beta-globin gene switching using a mini construct in transgenic mice." Molecular and Cellular Biology 12, no. 4 (1992): 1561–67. http://dx.doi.org/10.1128/mcb.12.4.1561-1567.1992.

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The developmental regulation of the human globin genes involves a key switch from fetal (gamma-) to adult (beta-) globin gene expression. It is possible to study the mechanism of this switch by expressing the human globin genes in transgenic mice. Previous work has shown that high-level expression of the human globin genes in transgenic mice requires the presence of the locus control region (LCR) upstream of the genes in the beta-globin locus. High-level, correct developmental regulation of beta-globin gene expression in transgenic mice has previously been accomplished only in 30- to 40-kb gen

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42

Lloyd, J. A., J. M. Krakowsky, S. C. Crable, and J. B. Lingrel. "Human gamma- to beta-globin gene switching using a mini construct in transgenic mice." Molecular and Cellular Biology 12, no. 4 (1992): 1561–67. http://dx.doi.org/10.1128/mcb.12.4.1561.

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The developmental regulation of the human globin genes involves a key switch from fetal (gamma-) to adult (beta-) globin gene expression. It is possible to study the mechanism of this switch by expressing the human globin genes in transgenic mice. Previous work has shown that high-level expression of the human globin genes in transgenic mice requires the presence of the locus control region (LCR) upstream of the genes in the beta-globin locus. High-level, correct developmental regulation of beta-globin gene expression in transgenic mice has previously been accomplished only in 30- to 40-kb gen

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43

Perkins, Andrew C., Michael Tallack, Ye Zhan, et al. "Ikaros Drives Human Haemoglobin Switching by Facilitating Active Chromatin Hub Formation." Blood 110, no. 11 (2007): 1772. http://dx.doi.org/10.1182/blood.v110.11.1772.1772.

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Abstract The human β globin locus consists of an upstream locus control region (LCR) and five functional genes arranged sequentially in the order of their expression during development: 5′-ε-Gγ-Aγ- δ- β-3′. Haemoglobin switching entails the successive recruitment of these genes into an active chromatin hub (ACH). Although much is known about the cis elements and transcription factors involved in globin gene regulation, less is known about ACH formation. Here we show that the transcription factor Ikaros plays an essential role in both the formation of the β-globin ACH, and in haemoglobin switch

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44

PERRINE, SUSAN P., DOUGLAS V. FALLER, PAUL SWERDLOW, et al. "Stopping the Biologic Clock for Globin Gene Switching." Annals of the New York Academy of Sciences 612, no. 1 Sixth Cooley' (1990): 134–40. http://dx.doi.org/10.1111/j.1749-6632.1990.tb24299.x.

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45

Russell, J. Eric, та Stephen A. Liebhaber. "Reversal of Lethal - and β-Thalassemias in Mice by Expression of Human Embryonic Globins". Blood 92, № 9 (1998): 3057–63. http://dx.doi.org/10.1182/blood.v92.9.3057.

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Abstract Genetic mutations that block - or β-globin gene expression in humans can result in severe and frequently lethal thalassemic phenotypes. Homozygous inactivation of the endogenous - or β-globin genes in mice results in corresponding thalassemic syndromes that are uniformly fatal in utero. In the current study, we show that the viability of these mice can be rescued by expression of human embryonic ζ- and -globins, respectively. The capacity of embryonic globins to fully substitute for their adult globin homologues is further demonstrated by showing that ζ- and -globins reverse the h

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46

Russell, J. Eric, та Stephen A. Liebhaber. "Reversal of Lethal - and β-Thalassemias in Mice by Expression of Human Embryonic Globins". Blood 92, № 9 (1998): 3057–63. http://dx.doi.org/10.1182/blood.v92.9.3057.421k57_3057_3063.

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Genetic mutations that block - or β-globin gene expression in humans can result in severe and frequently lethal thalassemic phenotypes. Homozygous inactivation of the endogenous - or β-globin genes in mice results in corresponding thalassemic syndromes that are uniformly fatal in utero. In the current study, we show that the viability of these mice can be rescued by expression of human embryonic ζ- and -globins, respectively. The capacity of embryonic globins to fully substitute for their adult globin homologues is further demonstrated by showing that ζ- and -globins reverse the hemolytic

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Kulozik, AE, A. Bellan-Koch, E. Kohne, and E. Kleihauer. "A deletion/inversion rearrangement of the beta-globin gene cluster in a Turkish family with delta beta zero-thalassemia intermedia." Blood 79, no. 9 (1992): 2455–59. http://dx.doi.org/10.1182/blood.v79.9.2455.2455.

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Abstract The most common forms of hereditary persistence of fetal hemoglobin synthesis (HPFH) and delta beta zero-thalassemia result from simple deletions of the beta-globin gene cluster or from point mutations in the gamma-globin gene promoters. These naturally occurring mutants extend our understanding of globin gene regulation and hemoglobin switching. Furthermore, they provide the opportunity to test in vivo hypothetical switching models that are based on the experimental approach. We report here a family with delta beta zero-thalassemia from Turkey with a complex rearrangement of the beta

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48

Kulozik, AE, A. Bellan-Koch, E. Kohne, and E. Kleihauer. "A deletion/inversion rearrangement of the beta-globin gene cluster in a Turkish family with delta beta zero-thalassemia intermedia." Blood 79, no. 9 (1992): 2455–59. http://dx.doi.org/10.1182/blood.v79.9.2455.bloodjournal7992455.

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The most common forms of hereditary persistence of fetal hemoglobin synthesis (HPFH) and delta beta zero-thalassemia result from simple deletions of the beta-globin gene cluster or from point mutations in the gamma-globin gene promoters. These naturally occurring mutants extend our understanding of globin gene regulation and hemoglobin switching. Furthermore, they provide the opportunity to test in vivo hypothetical switching models that are based on the experimental approach. We report here a family with delta beta zero-thalassemia from Turkey with a complex rearrangement of the beta-globin g

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49

Marini, Giuseppina M., Isadora Asunis, Annalisa Cabriolu, et al. "Delayed Embryonic to Adult Globin Switching in HMGB2 Knock Out Mice." Blood 118, no. 21 (2011): 2152. http://dx.doi.org/10.1182/blood.v118.21.2152.2152.

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Abstract Abstract 2152 Hypersensitive site 2 (HS2) of the locus control region (LCR) is required for the optimal regulation of the beta globin gene cluster. Screening a λgt11 cord blood cDNA library with the tandem NFE2 repeat of HS2 as recognition site probe, we isolated 14 cDNA clones of HMGB2, a chromatin non histone protein. Binding to the HS2 region was confirmed in vivo by ChIP assay. Transactivation analysis in K562 cells showed mild repression of a luciferase reporter driven by HS2 and the γ-promoter. The DNA bending capacity and the increased expression of HMGB2 during erythroid diffe

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Takayama, Naoya, Shiya Sano, Takafumi Shimizu, et al. "Epigenetic Memory Enables the Dominant Generation of Adult-Type Erythrocytes From Human Induced Pluripotent Stem Cells." Blood 116, no. 21 (2010): 648. http://dx.doi.org/10.1182/blood.v116.21.648.648.

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Abstract Abstract 648 It is well known that “globin switching” during erythropoiesis is associated with the pathophysiology of sickle cell anemia, as well as an approach to ameliorating some hemoglobinopathies. Furthermore, the process of globin switching represents an important paradigm for developmental gene regulation. Human embryonic stem cells (ESCs) and induced pluripotent stem cells (iPSCs) are attractive tools for studying the ontogeny of human erythropoiesis because they exhibit in vitro differentiation toward various erythrocytes with embryonic (e), fetal (g) or adult (b) globin gene

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