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Pesquisa : D12.776.124.400.434.325.374 [Categoria DeCS]
Referências encontradas : 21 [refinar]
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  1 / 21 MEDLINE  
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[PMID]:28154185
[Au] Autor:Wang Y; Wang Y; Ma L; Nie M; Ju J; Liu M; Deng Y; Yao B; Gui T; Li X; Guo C; Ma C; Tan R; Zhao Q
[Ad] Endereço:From the State Key Laboratory of Pharmaceutical Biotechnology, School of Life Sciences, Nanjing University, Nanjing 210023, China.
[Ti] Título:Heterochromatin Protein 1γ Is a Novel Epigenetic Repressor of Human Embryonic ϵ-Globin Gene Expression.
[So] Source:J Biol Chem;292(12):4811-4817, 2017 Mar 24.
[Is] ISSN:1083-351X
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Production of hemoglobin during development is tightly regulated. For example, expression from the human ß-globin gene locus, comprising ß-, δ-, ϵ-, and γ-globin genes, switches from ϵ-globin to γ-globin during embryonic development and then from γ-globin to ß-globin after birth. Expression of human ϵ-globin in mice has been shown to ameliorate anemia caused by ß-globin mutations, including those causing ß-thalassemia and sickle cell disease, raising the prospect that reactivation of ϵ-globin expression could be used in managing these conditions in humans. Although the human globin genes are known to be regulated by a variety of multiprotein complexes containing enzymes that catalyze epigenetic modifications, the exact mechanisms controlling ϵ-globin gene silencing remain elusive. Here we found that the heterochromatin protein HP1γ, a multifunctional chromatin- and DNA-binding protein with roles in transcriptional activation and elongation, represses ϵ-globin expression by interacting with a histone-modifying enzyme, lysine methyltransferase SUV4-20h2. Silencing of HP1γ expression markedly decreased repressive histone marks and the multimethylation of histone H3 lysine 9 and H4 lysine 20, leading to a significant decrease in DNA methylation at the proximal promoter of the ϵ-globin gene and greatly increased ϵ-globin expression. In addition, using chromatin immunoprecipitation, we showed that SUV4-20h2 facilitates the deposition of HP1γ on the ϵ-globin-proximal promoter. Thus, these data indicate that HP1γ is a novel epigenetic repressor of ϵ-globin gene expression and provide a potential strategy for targeted therapies for ß-thalassemia and sickle cell disease.
[Mh] Termos MeSH primário: Proteínas Cromossômicas não Histona/metabolismo
Repressão Epigenética
Globinas épsilon/genética
[Mh] Termos MeSH secundário: Linhagem Celular
Metilação de DNA
Histona-Lisina N-Metiltransferase/metabolismo
Seres Humanos
Regiões Promotoras Genéticas
Ativação Transcricional
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (CBX3 protein, human); 0 (Chromosomal Proteins, Non-Histone); 0 (epsilon-Globins); 107283-02-3 (heterochromatin-specific nonhistone chromosomal protein HP-1); EC 2.1.1.43 (Histone-Lysine N-Methyltransferase); EC 2.1.1.43 (SUV420H2 protein, human)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:170613
[Lr] Data última revisão:
170613
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170204
[St] Status:MEDLINE
[do] DOI:10.1074/jbc.M116.768515


  2 / 21 MEDLINE  
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[PMID]:27002261
[Au] Autor:McConaghy S; Manuel V; Nagji S; Ohls RK
[Ad] Endereço:Department of Pediatrics, University of New Mexico, Albuquerque, New Mexico.
[Ti] Título:Epsilon globin gene expression in developing human fetal tissues.
[So] Source:J Neonatal Perinatal Med;9(1):91-7, 2016.
[Is] ISSN:1878-4429
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:OBJECTIVE: The discovery of free fetal DNA in plasma of pregnant women has opened a new avenue for non-invasive prenatal diagnosis. We hypothesized that epsilon (É›)-globin gene expression could serve as a positive control for the presence of fetal nucleic acid. STUDY DESIGN: We measured É›-globin mRNA in human fetal tissues and compared concentrations with that measured in adult non-pregnant and pregnant samples. Total RNA was isolated from fetal marrow, liver, blood, and placenta (10-24 weeks gestation), from adult peripheral blood mononuclear cells, and from maternal plasma. RNA was reverse transcribed and quantitative polymerase chain reaction performed for É›-globin expression. RESULTS: É›-globin gene expression was detected in all fetal samples, was detected in plasma of pregnant women, but was negligible in non-pregnant samples. Relative É›-globin gene expression was significantly greater in fetal blood compared to fetal liver, and was minimally expressed in placenta. É›-globin gene expression decreased at the highest gestational ages in fetal blood, while expression was greatest at 15-19 weeks in fetal marrow. CONCLUSION: Fetal É›-globin gene expression is significantly greater than adult expression and is increased in maternal plasma compared to non-pregnant samples. É›-globin gene expression might serve as a positive control when determining the presence of fetal nucleic acid in total nucleic acid isolated from maternal plasma.
[Mh] Termos MeSH primário: Feto/metabolismo
Perfilação da Expressão Gênica
RNA Mensageiro/análise
RNA Mensageiro/sangue
Globinas épsilon/genética
[Mh] Termos MeSH secundário: Biomarcadores/análise
Biomarcadores/sangue
Feminino
Feto/embriologia
Idade Gestacional
Seres Humanos
Fígado/metabolismo
Especificidade de Órgãos
Placenta/metabolismo
Gravidez
Diagnóstico Pré-Natal
Padrões de Referência
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Biomarkers); 0 (RNA, Messenger); 0 (epsilon-Globins)
[Em] Mês de entrada:1705
[Cu] Atualização por classe:170523
[Lr] Data última revisão:
170523
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160323
[St] Status:MEDLINE
[do] DOI:10.3233/NPM-16915052


  3 / 21 MEDLINE  
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[PMID]:25488195
[Au] Autor:Zebisch A; Schulz E; Grosso M; Lombardo B; Acierno G; Sill H; Iolascon A
[Ad] Endereço:Division of Hematology, Medical University of Graz, Graz, Austria.
[Ti] Título:Identification of a novel variant of epsilon-gamma-delta-beta thalassemia highlights limitations of next generation sequencing.
[So] Source:Am J Hematol;90(3):E52-4, 2015 Mar.
[Is] ISSN:1096-8652
[Cp] País de publicação:United States
[La] Idioma:eng
[Mh] Termos MeSH primário: Talassemia/diagnóstico
Globinas beta/genética
Globinas delta/genética
Globinas épsilon/genética
gama-Globinas/genética
[Mh] Termos MeSH secundário: Sequenciamento de Nucleotídeos em Larga Escala
Seres Humanos
Masculino
Meia-Idade
Reação em Cadeia da Polimerase Multiplex
Mutação
Linhagem
Talassemia/genética
Talassemia/patologia
[Pt] Tipo de publicação:CASE REPORTS; LETTER; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (beta-Globins); 0 (delta-Globins); 0 (epsilon-Globins); 0 (gamma-Globins)
[Em] Mês de entrada:1504
[Cu] Atualização por classe:150218
[Lr] Data última revisão:
150218
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:141210
[St] Status:MEDLINE
[do] DOI:10.1002/ajh.23913


  4 / 21 MEDLINE  
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[PMID]:25107887
[Au] Autor:Trakarnsanga K; Wilson MC; Lau W; Singleton BK; Parsons SF; Sakuntanaga P; Kurita R; Nakamura Y; Anstee DJ; Frayne J
[Ad] Endereço:School of Biochemistry, University of Bristol, Bristol, United Kingdom Department of Biochemistry, Faculty of Medicine Siriraj Hospital, Mahidol University, Bangkok, Thailand.
[Ti] Título:Induction of adult levels of ß-globin in human erythroid cells that intrinsically express embryonic or fetal globin by transduction with KLF1 and BCL11A-XL.
[So] Source:Haematologica;99(11):1677-85, 2014 Nov.
[Is] ISSN:1592-8721
[Cp] País de publicação:Italy
[La] Idioma:eng
[Ab] Resumo:A major barrier to the clinical use of erythrocytes generated in vitro from pluripotent stem cells or cord blood progenitors is failure of these erythrocytes to express adult hemoglobin. The key regulators of globin switching KLF1 and BCL11A are absent or at a lower level than in adult cells in K562 and erythroid cells differentiated in vitro from induced pluripotent stem cells and cord blood progenitors. Transfection or transduction of K562 and cord blood erythroid cells with either KLF1 or BCL11A-XL had little effect on ß-globin expression. In contrast, transduction with both transcription factors stimulated ß-globin expression. Similarly, increasing the level of BCL11A-XL in the induced pluripotent stem cell-derived erythroid cell line HiDEP-1, which has levels of endogenous KLF1 similar to adult cells but lacks BCL11A, resulted in levels of ß-globin equivalent to that of adult erythroid cells. Interestingly, this increase in ß-globin was coincident with a decrease in ε- and ζ-, but not γ-globin, implicating BCL11A in repression of embryonic globin expression. The data show that KLF1 and BCL11A-XL together are required, but sufficient to induce adult levels of ß-globin in induced pluripotent stem cell and cord blood-derived erythroid cells that intrinsically express embryonic or fetal globin.
[Mh] Termos MeSH primário: Proteínas de Transporte/genética
Células Eritroides/metabolismo
Hemoglobina Fetal/genética
Expressão Gênica
Fatores de Transcrição Kruppel-Like/genética
Proteínas Nucleares/genética
Transdução Genética
Globinas beta/genética
[Mh] Termos MeSH secundário: Células-Tronco Adultas/citologia
Células-Tronco Adultas/metabolismo
Diferenciação Celular/genética
Linhagem Celular
Células Eritroides/citologia
Células-Tronco Hematopoéticas/citologia
Células-Tronco Hematopoéticas/metabolismo
Seres Humanos
Células-Tronco Pluripotentes Induzidas/citologia
Células-Tronco Pluripotentes Induzidas/metabolismo
Células K562
Fenótipo
Transfecção
Globinas épsilon/genética
gama-Globinas/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (BCL11A protein, human); 0 (Carrier Proteins); 0 (Kruppel-Like Transcription Factors); 0 (Nuclear Proteins); 0 (beta-Globins); 0 (epsilon-Globins); 0 (erythroid Kruppel-like factor); 0 (gamma-Globins); 9034-63-3 (Fetal Hemoglobin)
[Em] Mês de entrada:1507
[Cu] Atualização por classe:170922
[Lr] Data última revisão:
170922
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:140810
[St] Status:MEDLINE
[do] DOI:10.3324/haematol.2014.110155


  5 / 21 MEDLINE  
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[PMID]:24371119
[Au] Autor:Roosjen M; McColl B; Kao B; Gearing LJ; Blewitt ME; Vadolas J
[Ad] Endereço:1Cell and Gene Therapy Group, Murdoch Children's Research Institute, Royal Children's Hospital, Flemington Rd., Parkville, VIC 3052, Australia. jim.vadolas@mcri.edu.au.
[Ti] Título:Transcriptional regulators Myb and BCL11A interplay with DNA methyltransferase 1 in developmental silencing of embryonic and fetal ß-like globin genes.
[So] Source:FASEB J;28(4):1610-20, 2014 Apr.
[Is] ISSN:1530-6860
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The clinical symptoms of hemoglobin disorders such as ß-thalassemia and sickle cell anemia are significantly ameliorated by the persistent expression of γ-globin after birth. This knowledge has driven the discovery of important regulators that silence γ-globin postnatally. Improved understanding of the γ- to ß-globin switching mechanism holds the key to devising targeted therapies for ß-hemoglobinopathies. To further investigate this mechanism, we used the murine erythroleukemic (MEL) cell line containing an intact 183-kb human ß-globin locus, in which the (G)γ- and ß-globin genes are replaced by DsRed and eGFP fluorescent reporters, respectively. Following RNA interference (RNAi)-mediated knockdown of two key transcriptional regulators, Myb and BCL11A, we observed a derepression of γ-globin, measured by DsRed fluorescence and qRT-PCR (P<0.001). Interestingly, double knockdown of Myb and DNA methyltransferase 1 (DNMT1) resulted in a robust induction of ε-globin, (up to 20% of total ß-like globin species) compared to single knockdowns (P<0.001). Conversely, double knockdowns of BCL11A and DNMT1 enhanced γ-globin expression (up to 90% of total ß-like globin species) compared to single knockdowns (P<0.001). Moreover, following RNAi treatment, expression of human ß-like globin genes mirrored the expression levels of their endogenous murine counterparts. These results demonstrate that Myb and BCL11A cooperate with DNMT1 to achieve developmental repression of embryonic and fetal ß-like globin genes in the adult erythroid environment.
[Mh] Termos MeSH primário: Proteínas de Transporte/genética
DNA (Citosina-5-)-Metiltransferases/genética
Hemoglobina Fetal/genética
Proteínas Nucleares/genética
Proteínas Proto-Oncogênicas c-myb/genética
Interferência de RNA
[Mh] Termos MeSH secundário: Animais
Western Blotting
Proteínas de Transporte/metabolismo
Diferenciação Celular/genética
Linhagem Celular Tumoral
Proliferação Celular
DNA (Citosina-5-)-Metiltransferase 1
DNA (Citosina-5-)-Metiltransferases/metabolismo
Eritropoese/genética
Hemoglobina Fetal/metabolismo
Proteínas de Fluorescência Verde/genética
Proteínas de Fluorescência Verde/metabolismo
Seres Humanos
Leucemia Eritroblástica Aguda/genética
Leucemia Eritroblástica Aguda/metabolismo
Leucemia Eritroblástica Aguda/patologia
Proteínas Luminescentes/genética
Proteínas Luminescentes/metabolismo
Camundongos
Proteínas Nucleares/metabolismo
Proteínas Proto-Oncogênicas c-myb/metabolismo
Reação em Cadeia da Polimerase Via Transcriptase Reversa
Transgenes/genética
Globinas beta/genética
Globinas beta/metabolismo
Globinas épsilon/genética
Globinas épsilon/metabolismo
gama-Globinas/genética
gama-Globinas/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Bcl11a protein, mouse); 0 (Carrier Proteins); 0 (Luminescent Proteins); 0 (Nuclear Proteins); 0 (Proto-Oncogene Proteins c-myb); 0 (beta-Globins); 0 (enhanced green fluorescent protein); 0 (epsilon-Globins); 0 (fluorescent protein 583); 0 (gamma-Globins); 147336-22-9 (Green Fluorescent Proteins); 9034-63-3 (Fetal Hemoglobin); EC 2.1.1.37 (DNA (Cytosine-5-)-Methyltransferase 1); EC 2.1.1.37 (DNA (Cytosine-5-)-Methyltransferases); EC 2.1.1.37 (DNMT1 protein, human); EC 2.1.1.37 (Dnmt1 protein, mouse)
[Em] Mês de entrada:1406
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:131228
[St] Status:MEDLINE
[do] DOI:10.1096/fj.13-242669


  6 / 21 MEDLINE  
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[PMID]:24195361
[Au] Autor:Ma Y; Wang B; Gong B; Wang F; Zhao H; Zhang J; Yu J
[Ad] Endereço:State Key Laboratory of Medical Molecular Biology, Institute of Basic Medical Sciences, Chinese Academy of Medical Sciences (CAMS) & Peking Union Medical College (PUMC), Beijing 100005, China.
[Ti] Título:[MiR-24 improves beta-like globin gene expression through targeting Sp1].
[So] Source:Sheng Wu Gong Cheng Xue Bao;29(7):946-54, 2013 Jul.
[Is] ISSN:1000-3061
[Cp] País de publicação:China
[La] Idioma:chi
[Ab] Resumo:We studied the function and mechanism of miR-24 in regulating beta-like globin gene expression. We first detected the expression of miR-24 during erythroid differentiation and also detected the globin gene expression in miR-24 overexpressing K562 cells through q-PCR. Dual-luciferase reporter assay and Western blotting were used to identify target genes of miR-24. "Rescue experiment" was further used to investigate the regulation of miR-24 on globin gene expression whether depending on targeting Sp1 or not. We found that miR-24 increased during hemin-induced K562 cells and EPO-induced HPCs (hematopoietic progenitor cells) erythroid differentiation. Overexpression of miR-24 in K562 cells promoted the epsilon- and gamma-globin gene expression during hemin-induced erythroid differentiation through targeting the negative globin regulator Sp1. These results suggested that miR-24 can improve the expression of beta-like globin gene through targeting Sp1.
[Mh] Termos MeSH primário: Células-Tronco Hematopoéticas/metabolismo
MicroRNAs/genética
Fator de Transcrição Sp1/genética
Globinas épsilon/genética
gama-Globinas/genética
[Mh] Termos MeSH secundário: Diferenciação Celular
Regulação da Expressão Gênica
Seres Humanos
Células K562
[Pt] Tipo de publicação:ENGLISH ABSTRACT; JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (MIRN24 microRNA, human); 0 (MicroRNAs); 0 (Sp1 Transcription Factor); 0 (Sp1 protein, human); 0 (epsilon-Globins); 0 (gamma-Globins)
[Em] Mês de entrada:1505
[Cu] Atualização por classe:131107
[Lr] Data última revisão:
131107
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:131108
[St] Status:MEDLINE


  7 / 21 MEDLINE  
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[PMID]:23993951
[Au] Autor:Chang KH; Huang A; Han H; Jiang Y; Fang X; Song CZ; Padilla S; Wang H; Qu H; Stamatoyannopoulos J; Li Q; Papayannopoulou T
[Ad] Endereço:Division of Hematology, Department of Medicine, University of Washington, Seattle, WA, USA.
[Ti] Título:Transcriptional environment and chromatin architecture interplay dictates globin expression patterns of heterospecific hybrids derived from undifferentiated human embryonic stem cells or from their erythroid progeny.
[So] Source:Exp Hematol;41(11):967-979.e6, 2013 Nov.
[Is] ISSN:1873-2399
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:To explore the response of ß globin locus with established chromatin domains upon their exposure to new transcriptional environments, we transferred the chromatin-packaged ß globin locus of undifferentiated human embryonic stem cells (hESCs) or hESC-derived erythroblasts into an adult transcriptional environment. Distinct globin expression patterns were observed. In hESC-derived erythroblasts where both ε and γ globin were active and marked by similar chromatin modifications, ε globin was immediately silenced upon transfer, whereas γ globin continued to be expressed for months, implying that different transcriptional environments were required for their continuing expression. Whereas ß globin was silent both in hESCs and in hESC-derived erythroblasts, ß globin was only activated upon transfer from hESCs, but not in the presence of dominant γ globin transferred from hESC-derived erythroblasts, confirming the competing nature of γ versus ß globin expression. With time, however, silencing of γ globin occurred in the adult transcriptional environment with concurrent activation of ß-globin, accompanied by a drastic change in the epigenetic landscape of γ and ß globin gene regions without apparent changes in the transcriptional environment. This switching process could be manipulated by overexpression or downregulation of certain transcription factors. Our studies provide important insights into the interplay between the transcription environment and existing chromatin domains, and we offer an experimental system to study the time-dependent human globin switching.
[Mh] Termos MeSH primário: Cromatina/genética
Células-Tronco Embrionárias/metabolismo
Células Eritroides/metabolismo
Globinas/genética
[Mh] Termos MeSH secundário: Adulto
Animais
Azacitidina/análogos & derivados
Azacitidina/farmacologia
Proteínas de Transporte/genética
Proteínas de Transporte/metabolismo
Diferenciação Celular/genética
Linhagem Celular Tumoral
Células Cultivadas
Cromatina/metabolismo
Embrião de Mamíferos/citologia
Células-Tronco Embrionárias/citologia
Eritroblastos/citologia
Eritroblastos/metabolismo
Células Eritroides/citologia
Fibroblastos/citologia
Fibroblastos/metabolismo
Regulação da Expressão Gênica no Desenvolvimento/efeitos dos fármacos
Seres Humanos
Células Híbridas
Camundongos
Proteínas Nucleares/genética
Proteínas Nucleares/metabolismo
Análise de Sequência com Séries de Oligonucleotídeos
Interferência de RNA
Fatores de Tempo
Transcriptoma/efeitos dos fármacos
Transcriptoma/genética
Globinas beta/genética
Globinas épsilon/genética
gama-Globinas/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL
[Nm] Nome de substância:
0 (Bcl11a protein, mouse); 0 (Carrier Proteins); 0 (Chromatin); 0 (Nuclear Proteins); 0 (beta-Globins); 0 (epsilon-Globins); 0 (gamma-Globins); 776B62CQ27 (decitabine); 9004-22-2 (Globins); M801H13NRU (Azacitidine)
[Em] Mês de entrada:1401
[Cu] Atualização por classe:170220
[Lr] Data última revisão:
170220
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:130903
[St] Status:MEDLINE


  8 / 21 MEDLINE  
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[PMID]:23913596
[Au] Autor:Vacaru AM; Isern J; Fraser ST; Baron MH
[Ad] Endereço:Department of Medicine, The Icahn School of Medicine at Mount Sinai, New York, New York; The Tisch Cancer Institute, The Icahn School of Medicine at Mount Sinai, New York, New York.
[Ti] Título:Analysis of primitive erythroid cell proliferation and enucleation using a cyan fluorescent reporter in transgenic mice.
[So] Source:Genesis;51(11):751-62, 2013 Nov.
[Is] ISSN:1526-968X
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Primitive erythropoiesis is a vital process for mammalian embryonic development. Here we report the generation and characterization of a new transgenic mouse line that expresses a histone H2B-CFP fusion protein in the nuclei of primitive erythroid cells. We demonstrate the potential of this ε-globin-histone H2B-CFP line for multicolor imaging and flow cytometry analysis. The ε-globin-H2B-CFP line was used to analyze the cell cycle distribution and proliferation of CFP-expressing primitive erythroblasts from E8.5-E13.5. We also evaluated phagocytosis of extruded CFP-positive nuclei by macrophages in fetal liver and placenta. The ε-globin-H2B-CFP transgenic mouse line adds to the available tools for studying the development of the primitive erythroid lineage.
[Mh] Termos MeSH primário: Eritroblastos/fisiologia
Eritropoese
Proteínas de Fluorescência Verde/metabolismo
[Mh] Termos MeSH secundário: Animais
Linhagem da Célula
Núcleo Celular/fisiologia
Proliferação Celular
Embrião de Mamíferos
Eritroblastos/citologia
Eritropoese/genética
Genes Reporter
Genótipo
Histonas/genética
Histonas/metabolismo
Camundongos
Camundongos Transgênicos
Fagocitose
Proteínas Recombinantes de Fusão/metabolismo
Globinas épsilon/genética
Globinas épsilon/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL
[Nm] Nome de substância:
0 (Cyan Fluorescent Protein); 0 (Histones); 0 (Recombinant Fusion Proteins); 0 (epsilon-Globins); 147336-22-9 (Green Fluorescent Proteins)
[Em] Mês de entrada:1406
[Cu] Atualização por classe:161019
[Lr] Data última revisão:
161019
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:130806
[St] Status:MEDLINE
[do] DOI:10.1002/dvg.22420


  9 / 21 MEDLINE  
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[PMID]:22677107
[Au] Autor:Rooks H; Clark B; Best S; Rushton P; Oakley M; Thein OS; Cuthbert AC; Britland A; Ruf A; Thein SL
[Ad] Endereço:King's College London, Molecular Haematology, James Black Centre, London SE5 9NU, UK.
[Ti] Título:A novel 506kb deletion causing ÎµÎ³Î´ß thalassemia.
[So] Source:Blood Cells Mol Dis;49(3-4):121-7, 2012 Oct 15-Dec 15.
[Is] ISSN:1096-0961
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:We describe a novel deletion causing ÎµÎ³Î´ß thalassemia in a Pakistani family. The Pakistani deletion is 506kb in length, and the second largest ÎµÎ³Î´ß thalassemia deletion reported to date. It removes the entire ß globin gene (HBB) cluster, extending from 431kb upstream to 75kb downstream of the ε globin gene (HBE). The breakpoint junction occurred within a 160bp palindrome embedded in LINE/LTR repeats, and contained a short (9bp) region of direct homology which may have contributed to the recombination event. Characterization of the deletion breakpoints has been particularly challenging due to the complexity of DNA deletion, insertion and inversion, involving a multitude of methodologies, mirroring the changing DNA analysis technologies.
[Mh] Termos MeSH primário: Globinas beta/genética
Talassemia beta/genética
Globinas delta/genética
Talassemia delta/genética
Globinas épsilon/genética
gama-Globinas/genética
[Mh] Termos MeSH secundário: Adulto
Sequência de Bases
Pontos de Quebra do Cromossomo
Cromossomos Humanos Par 11
Feminino
Recombinação Homóloga
Seres Humanos
Lactente
Sequências Repetidas Invertidas
Elementos Nucleotídeos Longos e Dispersos
Masculino
Dados de Sequência Molecular
Família Multigênica
Análise de Sequência de DNA
Deleção de Sequência
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (beta-Globins); 0 (delta-Globins); 0 (epsilon-Globins); 0 (gamma-Globins)
[Em] Mês de entrada:1303
[Cu] Atualização por classe:170922
[Lr] Data última revisão:
170922
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:120609
[St] Status:MEDLINE
[do] DOI:10.1016/j.bcmd.2012.05.010


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[PMID]:22328728
[Au] Autor:Xue Z; Lv X; Song W; Wang X; Zhao GN; Wang WT; Xiong J; Mao BB; Yu W; Yang B; Wu J; Zhou LQ; Hao DL; Dong WJ; Liu DP; Liang CC
[Ad] Endereço:National Laboratory of Medical Molecular Biology, Institute of Basic Medical Sciences, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing 100005, PR China.
[Ti] Título:SIRT1 deacetylates SATB1 to facilitate MAR HS2-MAR ε interaction and promote ε-globin expression.
[So] Source:Nucleic Acids Res;40(11):4804-15, 2012 Jun.
[Is] ISSN:1362-4962
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:The higher order chromatin structure has recently been revealed as a critical new layer of gene transcriptional control. Changes in higher order chromatin structures were shown to correlate with the availability of transcriptional factors and/or MAR (matrix attachment region) binding proteins, which tether genomic DNA to the nuclear matrix. How posttranslational modification to these protein organizers may affect higher order chromatin structure still pending experimental investigation. The type III histone deacetylase silent mating type information regulator 2, S. cerevisiae, homolog 1 (SIRT1) participates in many physiological processes through targeting both histone and transcriptional factors. We show that MAR binding protein SATB1, which mediates chromatin looping in cytokine, MHC-I and ß-globin gene loci, as a new type of SIRT1 substrate. SIRT1 expression increased accompanying erythroid differentiation and the strengthening of ß-globin cluster higher order chromatin structure, while knockdown of SIRT1 in erythroid k562 cells weakened the long-range interaction between two SATB1 binding sites in the ß-globin locus, MAR(HS2) and MAR(ε). We also show that SIRT1 activity significantly affects ε-globin gene expression in a SATB1-dependent manner and that knockdown of SIRT1 largely blocks ε-globin gene activation during erythroid differentiation. Our work proposes that SIRT1 orchestrates changes in higher order chromatin structure during erythropoiesis, and reveals the dynamic higher order chromatin structure regulation at posttranslational modification level.
[Mh] Termos MeSH primário: Regulação da Expressão Gênica
Proteínas de Ligação à Região de Interação com a Matriz/metabolismo
Regiões de Interação com a Matriz
Sirtuína 1/metabolismo
Globinas épsilon/genética
[Mh] Termos MeSH secundário: Células Cultivadas
Células Eritroides/efeitos dos fármacos
Células Eritroides/metabolismo
Regulação da Expressão Gênica/efeitos dos fármacos
Hemina/farmacologia
Seres Humanos
Células K562
Região de Controle de Locus Gênico
Globinas beta/genética
Globinas épsilon/biossíntese
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Matrix Attachment Region Binding Proteins); 0 (SATB1 protein, human); 0 (beta-Globins); 0 (epsilon-Globins); 743LRP9S7N (Hemin); EC 3.5.1.- (Sirtuin 1)
[Em] Mês de entrada:1208
[Cu] Atualização por classe:150225
[Lr] Data última revisão:
150225
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:120214
[St] Status:MEDLINE
[do] DOI:10.1093/nar/gks064



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