ArticleBlood cells, molecules & diseases2011
Regulation of γ-globin gene expression involves signaling through the p38 MAPK/CREB1 pathway.
Article in Blood cells, molecules & diseases, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers, 1 of them a synthesis that pooled it.
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Who cites it
18 citing papers in PubMed, 1 synthesis or guideline pooled it, 31 citations in OpenAlex.
- A systematic review of known mechanisms of hydroxyurea-induced fetal hemoglobin for treatment of sickle cell disease.Expert review of hematology · 2015Pooled it
- Nobiletin protected against hypertrophic cardiomyopathy via targeting PPARα.Frontiers in pharmacology · 2025Article
- Transmembrane Protein ANTXR1 RegulatesJournal of immunology research · 2022Article
- Synthesis and pharmacological evaluation of pomalidomide derivatives useful for sickle cell disease treatment.Bioorganic chemistry · 2021Article
- Distinct miRNA Signatures and Networks Discern Fetal from Adult Erythroid Differentiation and Primary from Immortalized Erythroid Cells.International journal of molecular sciences · 2021Article
- Effects of CREB1 gene silencing on cognitive dysfunction by mediating PKA-CREB signaling pathway in mice with vascular dementia.Molecular medicine (Cambridge, Mass.) · 2018Article
- Article
- Butyrate regulates the expression of inflammatory and chemotactic cytokines in human acute leukemic cells during apoptosis.Cytokine · 2016Article
- Original Research: A case-control genome-wide association study identifies genetic modifiers of fetal hemoglobin in sickle cell disease.Experimental biology and medicine (Maywood, N.J.) · 2016Article
- Hydroxyurea down-regulates BCL11A, KLF-1 and MYB through miRNA-mediated actions to induce γ-globin expression: implications for new therapeutic approaches of sickle cell disease.Clinical and translational medicine · 2016Article
- Article
- Cell signaling pathways involved in drug-mediated fetal hemoglobin induction: Strategies to treat sickle cell disease.Experimental biology and medicine (Maywood, N.J.) · 2015Review
- Pharmacological Induction of Human Fetal Globin Gene in Hydroxyurea-Resistant Primary Adult Erythroid Cells.Molecular and cellular biology · 2015Article
- Hydroxyurea-inducible SAR1 gene acts through the Giα/JNK/Jun pathway to regulate γ-globin expression.Blood · 2014Article
- Characterization of transcription factor networks involved in umbilical cord blood CD34+ stem cells-derived erythropoiesis.PloS one · 2014Article
- Globin gene expression in correlation with G protein-related genes during erythroid differentiation.BMC genomics · 2013Article
- Regulation of Gγ-globin gene by ATF2 and its associated proteins through the cAMP-response element.PloS one · 2013Article
- Characterization of the transcriptome profiles related to globin gene switching during in vitro erythroid maturation.BMC genomics · 2012Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
In response to sodium butyrate and trichostatin A treatment in erythroid cells, p38 mitogen activated protein kinase (MAPK) mediates fetal hemoglobin (HbF) induction by activating cAMP response element binding protein 1 (CREB1). To expand on this observation, we completed studies to determine the role of p38 MAPK in steady-state γ-globin regulation. We propose that p38 signaling regulates Gγ-globin transcription during erythroid maturation through its downstream effector CREB1 which binds the Gγ-globin cAMP response element (G-CRE). We demonstrated that a loss of p38 or CREB1 function by siRNA knockdown resulted in target gene silencing. Moreover, gain of p38 or CREB1 function augments γ-globin transcription. These regulatory effects were conserved under physiological conditions tested in primary erythroid cells. When the G-CRE was mutated in a stable chromatin environment Gγ-globin promoter activity was nearly abolished. Furthermore, introduction of mutations in the G-CRE abolished Gγ-globin activation via p38 MAPK/CREB1 signaling. Chromatin immunoprecipitation assays (ChIP) demonstrated that CREB1 and its binding partner CREB binding protein (CBP) co-localize at the G-CRE region. These data support the role of p38 MAPK/CREB1 signaling in Gγ-globin gene transcription under steady-state conditions.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.