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Exploring Novel Strategies to Alleviate Symptoms of β-Globinopathies: Examining the Potential Role of Embryonic ε-globin Induction.
Transfus Med Rev
October 2024
Department of Pathology, Brigham and Women's Hospital, Boston, MA, United States. Electronic address:
Article Synopsis
- β-thalassemia and sickle cell disease are common genetic blood disorders caused by mutations in the β-globin gene, leading to anemia and requiring treatments like blood transfusions and bone marrow transplants.
- New research is exploring the potential of inducing ε-globin expression, which was previously thought non-inducible postnatally, as a way to improve treatment outcomes for these conditions.
- The review highlights the need for further research into the mechanisms of ε-globin silencing and suggests future drug development initiatives to harness its therapeutic benefits.
AZD8055 Is More Effective Than Rapamycin in Inhibiting Proliferation and Promoting Mitochondrial Clearance in Erythroid Differentiation.
Anal Cell Pathol (Amst)
October 2024
Shantou University Medical College, Shantou, Guangdong Province, China.
Article Synopsis
- mTOR plays a crucial role in various cellular processes, including erythropoiesis, and consists of two complexes, mTORC1 and mTORC2, which have different functions and effects in signaling.
- Previous research indicated that inhibiting mTORC1 with rapamycin affected early erythroid progenitor expansion and later stages of erythroid differentiation.
- This study compared the effects of two inhibitors (AZD8055 and rapamycin) on erythroid differentiation in cell and mouse models, finding that both increased specific erythroid markers, with AZD8055 being more effective at suppressing cell proliferation and promoting mitochondrial clearance than rapamycin.
The anti-SARS-CoV-2 BNT162b2 vaccine suppresses mithramycin-induced erythroid differentiation and expression of embryo-fetal globin genes in human erythroleukemia K562 cells.
Exp Cell Res
December 2023
Department of Life Sciences and Biotechnology, Section of Biochemistry and Molecular Biology, University of Ferrara, 44121 Ferrara, Italy; Center 'Chiara Gemmo and Elio Zago' for the Research on Thalassemia, University of Ferrara, 44121 Ferrara, Italy. Electronic address:
The severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is causative of the ongoing coronavirus disease 2019 (COVID-19) pandemic. The SARS-CoV-2 Spike protein (S-protein) plays an important role in the early phase of SARS-CoV-2 infection through efficient interaction with ACE2. The S-protein is produced by RNA-based COVID-19 vaccines, that were fundamental for the reduction of the viral spread within the population and the clinical severity of COVID-19.
View Article and Find Full Text PDFmiR-365-3p mediates BCL11A and SOX6 erythroid-specific coregulation: A new player in HbF activation.
Mol Ther Nucleic Acids
December 2023
Istituto Di Ricerca Genetica e Biomedica del Consiglio Nazionale Delle Ricerche (IRGB-CNR), 09042 Monserrato, Italy.
Hemoglobin switching is a complex biological process not yet fully elucidated. The mechanism regulating the suppression of fetal hemoglobin (HbF) expression is of particular interest because of the positive impact of HbF on the course of diseases such as β-thalassemia and sickle cell disease, hereditary hemoglobin disorders that affect the health of countless individuals worldwide. Several transcription factors have been implicated in the control of HbF, of which BCL11A has emerged as a major player in HbF silencing.
View Article and Find Full Text PDFTargeted deletion of 5'HS2 enhancer of β-globin locus control region in K562 cells.
Yi Chuan
September 2022
Center for Comparative Biomedicine, Key laboratory of Systems Biomedicine (Ministry of Education), Institute of Systems Biomedicine, Shanghai Jiao Tong University, Shanghai 200240, China.
Human β-thalassemia is closely associated with aberrant expression of β-like globin genes. Human β-like globin genes are organized in the order of 5'-ε-Gγ-Aγ-δ-β-3' within the β-globin locus. The expression of β-like globin genes is regulated by 3'HS1 and five DNase I hypersensitive sites (5'HS5~5'HS1) in a locus control region.
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