Category Ranking
98%
Total Visits
921
Avg Visit Duration
2 minutes
Citations
20
Article Abstract
Upstream stimulatory factor and TFII-I are ubiquitously expressed helix-loop-helix transcription factors that interact with E-box sequences and or initiator elements. We previously demonstrated that upstream stimulatory factor is an activator of beta-globin gene expression whereas TFII-I is a repressor. In the present study, we demonstrate that upstream stimulatory factor interacts with the coactivator p300 and that this interaction is restricted to erythroid cells expressing the adult beta-globin gene. Furthermore, we demonstrate that Suz12, a component of the polycomb repressor complex 2, is recruited to the beta-globin gene. Reducing expression of Suz12 significantly activates beta-globin gene expression in an erythroid cell line with an embryonic phenotype. Suz12 also interacts with the adult beta-globin gene during early stages of erythroid differentiation of mouse embryonic stem cells. Our data suggest that TFII-I contributes to the recruitment of the polycomb repressor complex 2 complex to the beta-globin gene. Together, these data demonstrate that the antagonistic activities of upstream stimulatory factor and TFII-I on beta-globin gene expression are mediated at least in part by protein complexes that render the promoter associated chromatin accessible or inaccessible for the transcription complex.
Download full-text PDF |
Source |
|---|---|
| http://dx.doi.org/10.1111/j.1742-4658.2007.06128.x | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
Sickle cell disease: understanding pathophysiology, clinical features and advances in gene therapy approaches.
Front Pharmacol
August 2025
Department of Pharmacy, Faculty of Pharmacy and Health Sciences, Royal College of Medicine Perak, Universiti Kuala Lumpur, Ipoh, Malaysia.
Sickle cell disease (SCD) is an inherited blood disorder marked by the production of abnormal hemoglobin, leading to the distortion-or sickling-of red blood cells. The SCD arises from a single-point mutation that substitutes glutamic acid with valine at the sixth codon of the β-globin chain in hemoglobin. This substitution promotes deoxyhemoglobin aggregation, elevating red blood cell stiffness, and triggering vaso-occlusive and hemolytic repercussions.
View Article and Find Full Text PDFTotal ginsenosides enhance γ-globin expression and fetal hemoglobin production in β-thalassemia models.
Front Pharmacol
August 2025
Department of Medical Genetics, NHC Key Laboratory of Healthy Birth and Birth Defect Prevention in Western China, The First People's Hospital of Yunnan Province, Kunming, China.
Introduction: β-thalassemia is a genetic hemoglobinopathy characterized by defective β-globin synthesis and ineffective erythropoiesis. Pharmacological induction of fetal hemoglobin (HbF) via γ-globin gene activation represents a promising therapeutic strategy. Total ginsenosides (TG), the principal active constituents of , have shown epigenetic and transcriptional modulatory properties, yet their role in HbF induction remains unexplored.
View Article and Find Full Text PDFA Dual-Target Real-time PCR for proactive detection of Mpox variants.
J Virol Methods
September 2025
British Columbia Centre for Disease Control Public Health Laboratory, Vancouver, British Columbia, Canada; Department of Pathology and Laboratory Medicine, University of British Columbia, Vancouver, British Columbia, Canada. Electronic address:
In 2022, cases of Monkeypox virus (MPXV) in California contained a mutation in the TNF receptor gene (GR2G) that rendered the virus undetectable using a widely adopted public health diagnostic qPCR assay. This underscored the need for a dual-target PCR approach and prompted validation of a second target by the BCCDC Public Health Laboratory. In addition to the GR2G target validated in the original qPCR assay (and duplexed with the endogenous target human β-globin (HBG)), GP113 (OPG128) was identified and validated using both clinical samples and MPXV DNA controls.
View Article and Find Full Text PDFClinical and hematological characteristics of beta-plus thalassemia and uncommon beta-chain hemoglobin variants in Northern Thailand.
Ann Med
December 2025
Division of Hematology and Oncology, Department of Pediatrics, Faculty of Medicine, Chiang Mai University, Chiang Mai, Thailand.
Background: Thalassemia is the most common hereditary anemia worldwide. Beta-thalassemia results from mutations in gene, causing either absent (β) or decreased (β) production of β-globin. Mutations causing β-thalassemia comprise 10-20%of mutations in Thailand.
View Article and Find Full Text PDFTranscriptome analysis of unmedicated heterozygous familial Mediterranean fever patients reveals a type I interferon signature driving increasing Pyrin expression.
Ann Rheum Dis
August 2025
Department of Pediatrics, Division of Pediatric Rheumatology, Hacettepe University Faculty of Medicine, Ankara, Türkiye; Translational Medicine Laboratories, Pediatric Rheumatology Unit, Hacettepe University, Ankara, Türkiye. Electronic address:
Objectives: Familial Mediterranean fever (FMF) is traditionally viewed as an autosomal recessive autoinflammatory disorder. However, a significant subset of patients harbouring a single pathogenic MEFV mutation exhibit a clinical phenotype indistinguishable from that of homozygous patients. We aimed to compare the transcriptomic profiles of patients carrying a single pathogenic mutation who exhibit the classical FMF phenotype with those of healthy carriers (with 1 pathogenic mutation), as well as with homozygous or compound heterozygous patients (with 2 pathogenic mutations), to identify differential molecular signatures and potential diagnostic pathways.
View Article and Find Full Text PDF