DNA polymorphisms at the BCL11A, HBS1L-MYB, and beta-globin loci associate with fetal hemoglobin levels and pain crises in sickle cell disease.
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Haploinsufficiency for the erythroid transcription factor KLF1 causes hereditary persistence of fetal hemoglobinCurrent and future alternative therapies for beta-thalassemia majorCustomizing the genome as therapy for the β-hemoglobinopathiesNew insights from monogenic diabetes for "common" type 2 diabetesGenomic approaches to identifying targets for treating β hemoglobinopathiesFetal globin gene repressors as drug targets for molecular therapies to treat the β-globinopathiesBeta-globin gene haplotypes among cameroonians and review of the global distribution: is there a case for a single sickle mutation origin in Africa?Epigenetic regulation of fetal globin gene expression in adult erythroid cellsSickle cell disease and H3Africa: enhancing genomic research on cardiovascular diseases in African patientsErythro-megakaryocytic transcription factors associated with hereditary anemiaDevelopmental and species-divergent globin switching are driven by BCL11ANovel Inducers of Fetal Globin Identified through High Throughput Screening (HTS) Are Active In Vivo in Anemic Baboons and Transgenic MiceGlobal genetic architecture of an erythroid quantitative trait locus, HMIP-2Perspectives in Genetics and Sickle Cell Disease Prevention in Africa: Beyond the Preliminary Data from CameroonHemoglobin switching's surprise: the versatile transcription factor BCL11A is a master repressor of fetal hemoglobin.Genetic variation on chromosome 6 influences F cell levels in healthy individuals of African descent and HbF levels in sickle cell patients.Genetic modifiers of Hb E/beta0 thalassemia identified by a two-stage genome-wide association study.Chemical genetic strategy identifies histone deacetylase 1 (HDAC1) and HDAC2 as therapeutic targets in sickle cell disease.Acute chest syndrome is associated with single nucleotide polymorphism-defined beta globin cluster haplotype in children with sickle cell anaemia.Future alternative therapies for β-thalassemia.SAR1a promoter polymorphisms are not associated with fetal hemoglobin in patients with sickle cell disease from Cameroon.Fetal hemoglobin in sickle cell anemia: genome-wide association studies suggest a regulatory region in the 5' olfactory receptor gene clusterA genome-wide association study of red blood cell traits using the electronic medical record.Transcriptional silencing of {gamma}-globin by BCL11A involves long-range interactions and cooperation with SOX6.Sickle Cell Disease in the Post Genomic Era: A Monogenic Disease with a Polygenic Phenotype.Identification and characterization of small-molecule inducers of fetal hemoglobin.A call for policy action in sub-Saharan Africa to rethink diagnostics for pregnancy affected by sickle cell disease: differential views of medical doctors, parents and adult patients predict value conflicts in Cameroon.Sickle cell disease in Saudi Arabia: the phenotype in adults with the Arab-Indian haplotype is not benign.Role of the GATA-1/FOG-1/NuRD pathway in the expression of human beta-like globin genes.How I use hydroxyurea to treat young patients with sickle cell anemia.Genetic modifiers of the severity of sickle cell anemia identified through a genome-wide association studyFOETAL HAEMOGLOBIN (HbF) STATUS IN ADULT SICKLE CELL ANAEMIA PATIENTS IN IBADAN, NIGERIAAmelioration of Sardinian beta0 thalassemia by genetic modifiers.Fetal globin expression is regulated by Friend of Prmt1.Genetics of fetal hemoglobin in Tanzanian and British patients with sickle cell anemia.Genome-wide association study identifies genetic variants influencing F-cell levels in sickle-cell patients.Hydroxyurea treatment in β-thalassemia patients: to respond or not to respond?Genetic modifiers of HbF and response to hydroxyurea in sickle cell disease.Genome wide association study of fetal hemoglobin in sickle cell anemia in Tanzania.Induction of adult levels of β-globin in human erythroid cells that intrinsically express embryonic or fetal globin by transduction with KLF1 and BCL11A-XL
P2860
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P2860
DNA polymorphisms at the BCL11A, HBS1L-MYB, and beta-globin loci associate with fetal hemoglobin levels and pain crises in sickle cell disease.
description
2008 nî lūn-bûn
@nan
2008年の論文
@ja
2008年論文
@yue
2008年論文
@zh-hant
2008年論文
@zh-hk
2008年論文
@zh-mo
2008年論文
@zh-tw
2008年论文
@wuu
2008年论文
@zh
2008年论文
@zh-cn
name
DNA polymorphisms at the BCL11 ...... crises in sickle cell disease.
@ast
DNA polymorphisms at the BCL11 ...... crises in sickle cell disease.
@en
type
label
DNA polymorphisms at the BCL11 ...... crises in sickle cell disease.
@ast
DNA polymorphisms at the BCL11 ...... crises in sickle cell disease.
@en
prefLabel
DNA polymorphisms at the BCL11 ...... crises in sickle cell disease.
@ast
DNA polymorphisms at the BCL11 ...... crises in sickle cell disease.
@en
P2093
P2860
P50
P356
P1476
DNA polymorphisms at the BCL11 ...... crises in sickle cell disease.
@en
P2093
Aderson S Araújo
Antonio Cao
Fernando F Costa
Guillaume Lettre
Joel N Hirschhorn
Marcos André C Bezerra
Stuart H Orkin
Vijay G Sankaran
P2860
P304
11869-11874
P356
10.1073/PNAS.0804799105
P407
P577
2008-07-30T00:00:00Z